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Fang Y, Fan C, Li Y, Xie H. The influence of Helicobacter pylori infection on acute coronary syndrome and lipid metabolism in the Chinese ethnicity. Front Cell Infect Microbiol 2024; 14:1437425. [PMID: 39290976 PMCID: PMC11405380 DOI: 10.3389/fcimb.2024.1437425] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/27/2024] [Accepted: 08/16/2024] [Indexed: 09/19/2024] Open
Abstract
Background Acute coronary syndrome (ACS) patients frequently present a relatively high prevalence of Helicobacter pylori (H. pylori) infection. H. pylori was previously hypothesized to induce ACS through the regulation of lipid levels. However, the risk of H. pylori-induced ACS varies significantly among different ethnic groups, and the associations between H. pylori and lipid parameters remain unclear. This study aimed to systematically assess the risk of ACS in Chinese populations with H. pylori infection while also evaluating the effects of H. pylori on lipid parameters. Materials and methods A hospital-based case-control study involving 280 participants was conducted. Immunoblotting was used for the detection and genotyping of H. pylori. The associations between H. pylori and ACS, as well as lipid parameters, were analyzed via the chi-square test and a multiple logistic regression model. Results H. pylori infection significantly increased the risk of ACS among all participants (adjusted odds ratio (OR) = 4.04, 95% confidence interval (CI): 1.76-9.25, P < 0.05), with no associations with virulence factors (cytotoxin-associated gene A (CagA) or vacuole toxin geneA (VacA)). Subgroup analysis revealed a significant increase in the risk of ACS among the elderly population aged 56-64 years with H. pylori infection. Additionally, a substantial association was observed between H. pylori and acute myocardial infarction (AMI). No significant differences were found in lipid parameters, including low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and the LDL/HDL ratio, between individuals positive and negative for H. pylori infection. Similar results were observed between the ACS group and the control group. Conclusions Our study has demonstrated for the first time that H. pylori does not significantly impact lipid metabolism but increases the risk of ACS fourfold in the Chinese population (OR = 4.04, 95% CI: 1.76-9.25). Furthermore, the virulence factors of H. pylori (CagA and VacA) may not be involved in the mechanisms by which they promote the development of ACS. This finding provides additional evidence for the association between H. pylori and ACS among different ethnic groups and refutes the biological mechanism by which H. pylori affects ACS through lipid metabolism regulation. Regular screening for H. pylori and eradication treatment in elderly individuals and those at high risk for ACS may be effective measures for reducing the incidence of ACS. Future research should include multicenter randomized controlled trials and explore host genetics and the effects of H. pylori on the gut microbiota as potential biological pathways linking H. pylori and ACS.
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Affiliation(s)
- Yizhen Fang
- Department of Clinical Laboratory, Xiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China
- Department of Clinical Laboratory, Xiamen Key Laboratory of Precision Medicine for Cardiovascular Disease, Xiamen, China
| | - Chunming Fan
- Department of Clinical Laboratory, Xiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China
- Department of Clinical Laboratory, Xiamen Key Laboratory of Precision Medicine for Cardiovascular Disease, Xiamen, China
| | - Yun Li
- Blood Transfusion Department, Affiliated Fuzhou First Hospital of Fujian Medical University, Fuzhou, China
| | - Huabin Xie
- Department of Clinical Laboratory, Xiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China
- Department of Clinical Laboratory, Xiamen Key Laboratory of Precision Medicine for Cardiovascular Disease, Xiamen, China
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Sadighi A, Aghamohammadpour Z, Sadeghpour Heravi F, Somi MH, Masnadi Shirazi Nezhad K, Hosseini S, Bahman Soufiani K, Ebrahimzadeh Leylabadlo H. The protective effects of Helicobacter pylori: A comprehensive review. JOURNAL OF RESEARCH IN CLINICAL MEDICINE 2024; 12:17. [DOI: 10.34172/jrcm.34509] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2023] [Accepted: 10/15/2023] [Indexed: 01/03/2025] Open
Abstract
Previous reports have estimated that approximately half of the world’s population is infected with Helicobacter pylori, the most prevalent infectious agent responsible for gastrointestinal illnesses. Due to the life-threatening effects of H. pylori infections, numerous studies have focused on developing medical therapies for H. pylori infections, while the commensal relationship and positive impacts of this bacterium on overall human health have been largely overlooked. The inhibitory efficacy of H. pylori on the progression of several chronic inflammatory disorders and gastrointestinal diseases has recently raised concerns about whether this bacterium should be eradicated in affected individuals or maintained in an appropriate balance depending on the patient’s condition. This review investigates the beneficial effects of H. pylori in preventing various diseases and discusses the potential association of conditions such as inflammatory disorders with the absence of H. pylori.
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Affiliation(s)
- Ali Sadighi
- Liver and Gastrointestinal Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
| | - Zahra Aghamohammadpour
- Liver and Gastrointestinal Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
| | | | - Mohammad Hossein Somi
- Liver and Gastrointestinal Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
| | | | - Samaneh Hosseini
- Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
| | - Katayoun Bahman Soufiani
- Department of Laboratory Sciences and Microbiology, Faculty of Medical Sciences, Tabriz Medical Sciences, Islamic Azad University, Tabriz, Iran
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Luque EM, Díaz-Luján CM, Paira DA, de Loredo N, Torres PJ, Cantarelli VI, Fretes R, Motrich RD, Martini AC. Ghrelin misbalance affects mice embryo implantation and pregnancy success by uterine immune dysregulation and nitrosative stress. Front Endocrinol (Lausanne) 2023; 14:1288779. [PMID: 38107518 PMCID: PMC10722256 DOI: 10.3389/fendo.2023.1288779] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/04/2023] [Accepted: 11/09/2023] [Indexed: 12/19/2023] Open
Abstract
Introduction In a previous study we found that ghrelin (Ghrl) misbalance during the peri-implantation period significantly impaired fetus development. In this study we aimed to evaluate the putative mechanisms underlying these effects, including embryo implantation success, uterine nitric oxide synthase (NOS) activity, nitric oxide synthesis and the inflammatory/immune uterine profile. Methods Ghrelin misbalance was induced by injecting 4nmol/animal/day of Ghrl (hyperghrelinemia) or 6nmol/animal/day of a Ghrl antagonist (Ant: (D-Lys3)GHRP-6) from day 3 to 8 of pregnancy. Control animals (C) were injected with de vehicle. Females were euthanized at pregnancy day 8 and their uteri excised in order to evaluate: the percentage of reabsorbed embryos (microscopically), eNOS, iNOS and nytrotirosine expression (by immunohistochemistry), nitrite synthesis (by Griess technique), VEGF, IL-10, IL-17, IL-6, MMP9 and GM-CSF expression (by qPCR) and leukocyte infiltration by flow cytometry (evaluating T cells, NK cells, granulocytes, dendritic cells and macrophages). Results Ant-treatment significantly increased the percentage of reabsorbed embryos and the uterine expression of eNOS, iNOS and nytrotirosine. (D-Lys3)GHRP-6-treatment increased also the expression of the inflammatory cytokines IL-6, IL-17 and MMP9, and decreased that of IL-10 (anti-inflammatory). Moreover, Ant-treatment increased also the NK cells population and that of CD11b+ dendritic cells; and decreased T cells percentages. Similarly, hyperghrelinemia showed a significant increase vs. C on eNOS, iNOS and nytrotirosineuterine expression and a decrease in T cells percentages. Conclusion Ghrl misbalance during the peri-implantation period induces pro-inflammatory changes and nitrosative stress in the gravid uterus, impairing significantly embryo implantation and/or development.
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Affiliation(s)
- Eugenia Mercedes Luque
- Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
- Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/Universidad Nacional de Córdoba (UNC), Córdoba, Argentina
| | - Cintia María Díaz-Luján
- Instituto de Biología Celular, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
| | - Daniela Andrea Paira
- Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina
- Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/Universidad Nacional de Córdoba (UNC), Córdoba, Argentina
| | - Nicolás de Loredo
- Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
| | - Pedro Javier Torres
- Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
- Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/Universidad Nacional de Córdoba (UNC), Córdoba, Argentina
| | - Verónica Inés Cantarelli
- Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
- Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/Universidad Nacional de Córdoba (UNC), Córdoba, Argentina
| | - Ricardo Fretes
- Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/Universidad Nacional de Córdoba (UNC), Córdoba, Argentina
- Instituto de Biología Celular, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
| | - Rubén Darío Motrich
- Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina
- Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/Universidad Nacional de Córdoba (UNC), Córdoba, Argentina
| | - Ana Carolina Martini
- Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
- Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)/Universidad Nacional de Córdoba (UNC), Córdoba, Argentina
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Sharma P, Phatak SM, Warikoo P, Mathur A, Mahant S, Das K, Das R. Crosstalk between Helicobacter pylori and gastrointestinal microbiota in various gastroduodenal diseases-A systematic review. 3 Biotech 2023; 13:303. [PMID: 37588796 PMCID: PMC10425313 DOI: 10.1007/s13205-023-03734-5] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/20/2022] [Accepted: 07/21/2023] [Indexed: 08/18/2023] Open
Abstract
Gastroduodenal diseases have prevailed for a long time and more so due to dominance of gut bacteria Helicobacter pylori in most of the cases. But habitation by other gut microbiota in gastroduodenal diseases and the relationship between Helicobacter pylori and gastrointestinal microbiota in different gastroduodenal diseases is somewhat being unravelled in the current times. For this systematic review, we did a literature search of various gastroduodenal diseases and the effect on gut microbiota pertaining to it. A search of the online bibliographic databases PUBMED and PUBMED CENTRAL was carried out to identify articles published between 1977 and May 2022. The analysis of these selected studies highlighted the inhabitation of other gut microbiota such as Fusobacteria, Bacteroidetes, Streptococcaceae, Prevotellaceae, Fusobacteriaceae, and many others. Interplay between these microbiota and H. pylori have also been noted which suggested that gastroduodenal diseases and gut microbiota are intertwined by a symbiotic association regardless of the H. pylori status. The relationship between the gut microbiota and many gastroduodenal diseases, such as gastritis, gastric cancer, lymphomas, and ulcers, demonstrates the dysbiosis of the gut microbiota in both the presence and absence of H. pylori. The evolving ways for eliminating H. pylori are provided along with inhibiting qualities of other species on H. pylori. Most significant member of our gut system is Helicobacter pylori which has been associated with numerous diseases like gastric cancer, gastritis, duodenal ulcer.
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Affiliation(s)
- Prateek Sharma
- Center for Medical Biotechnology, Amity Institute of Biotechnology, Amity University, Noida, U.P. India
| | - Shravani M. Phatak
- Center for Medical Biotechnology, Amity Institute of Biotechnology, Amity University, Noida, U.P. India
| | - Prisha Warikoo
- Center for Medical Biotechnology, Amity Institute of Biotechnology, Amity University, Noida, U.P. India
| | - Akshita Mathur
- Center for Medical Biotechnology, Amity Institute of Biotechnology, Amity University, Noida, U.P. India
| | - Shweta Mahant
- Center for Medical Biotechnology, Amity Institute of Biotechnology, Amity University, Noida, U.P. India
| | - Kunal Das
- Department of Gastroenterology, Yashoda Super Speciality Hospital, Kaushambi, Ghaziabad, Uttar Pradesh India
| | - Rajashree Das
- Center for Medical Biotechnology, Amity Institute of Biotechnology, Amity University, Noida, U.P. India
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Xiong C, Zhao R, Xu J, Liang H, Zhang J, Huang Y, Luo X. Is Helicobacter pylori infection associated with osteoporosis? a systematic review and meta-analysis. J Bone Miner Metab 2023; 41:74-87. [PMID: 36348162 DOI: 10.1007/s00774-022-01379-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/20/2022] [Accepted: 10/12/2022] [Indexed: 11/09/2022]
Abstract
INTRODUCTION This study used systematic review and meta-analysis to evaluate the association between Helicobacter pylori infection and osteoporosis. MATERIALS AND METHODS PubMed, Ovid and Web of Science were searched to include observational studies published in English comparing bone mineral density changes between Helicobacter pylori-positive and -negative participants. The quality of the included literature was assessed using the Newcastle-Ottawa Quality Assessment Scale (NOS). R software was used for meta-analysis, and odds ratio (OR) and 95% confidence interval (CI) were calculated to evaluate the relationship between Helicobacter pylori infection and osteoporosis. RESULTS Twenty-two studies involving 24,176 participants were included in the study. Our meta-analysis showed that Helicobacter pylori infection was significantly associated with the risk of osteoporosis (OR: 1.12, 95%CI: 1.03, 1.22). Participants infected with the CagA-positive Helicobacter pylori strain were more likely to develop osteoporosis (OR = 1.42, 95%CI: 1.09; 1.85). CONCLUSION Infection with Helicobacter pylori, particularly the CagA-positive strain, has been associated with an increased risk of osteoporosis. The bone health of Helicobacter pylori-positive patients deserves more attention.
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Affiliation(s)
- Chuang Xiong
- Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1, Youyi Road, Yuan Jiagang, Yuzhong District, Chongqing, 400016, People's Republic of China
| | - Runhan Zhao
- Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1, Youyi Road, Yuan Jiagang, Yuzhong District, Chongqing, 400016, People's Republic of China
| | - Jingtao Xu
- Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1, Youyi Road, Yuan Jiagang, Yuzhong District, Chongqing, 400016, People's Republic of China
| | - Hao Liang
- Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1, Youyi Road, Yuan Jiagang, Yuzhong District, Chongqing, 400016, People's Republic of China
| | - Jun Zhang
- Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1, Youyi Road, Yuan Jiagang, Yuzhong District, Chongqing, 400016, People's Republic of China
| | - Yanran Huang
- Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1, Youyi Road, Yuan Jiagang, Yuzhong District, Chongqing, 400016, People's Republic of China
| | - Xiaoji Luo
- Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, No. 1, Youyi Road, Yuan Jiagang, Yuzhong District, Chongqing, 400016, People's Republic of China.
- Orthopedic Laboratory of Chongqing Medical University, Chongqing, People's Republic of China.
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Singh V, Rai R, Mathew BJ, Chourasia R, Singh AK, Kumar A, Chaurasiya SK. Phospholipase C: underrated players in microbial infections. Front Cell Infect Microbiol 2023; 13:1089374. [PMID: 37139494 PMCID: PMC10149971 DOI: 10.3389/fcimb.2023.1089374] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2022] [Accepted: 03/21/2023] [Indexed: 05/05/2023] Open
Abstract
During bacterial infections, one or more virulence factors are required to support the survival, growth, and colonization of the pathogen within the host, leading to the symptomatic characteristic of the disease. The outcome of bacterial infections is determined by several factors from both host as well as pathogen origin. Proteins and enzymes involved in cellular signaling are important players in determining the outcome of host-pathogen interactions. phospholipase C (PLCs) participate in cellular signaling and regulation by virtue of their ability to hydrolyze membrane phospholipids into di-acyl-glycerol (DAG) and inositol triphosphate (IP3), which further causes the activation of other signaling pathways involved in various processes, including immune response. A total of 13 PLC isoforms are known so far, differing in their structure, regulation, and tissue-specific distribution. Different PLC isoforms have been implicated in various diseases, including cancer and infectious diseases; however, their roles in infectious diseases are not clearly understood. Many studies have suggested the prominent roles of both host and pathogen-derived PLCs during infections. PLCs have also been shown to contribute towards disease pathogenesis and the onset of disease symptoms. In this review, we have discussed the contribution of PLCs as a determinant of the outcome of host-pathogen interaction and pathogenesis during bacterial infections of human importance.
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Affiliation(s)
- Vinayak Singh
- Molecular Signalling Lab, Department of Biological Science and Engineering, Maulana Azad National Institute of Technology, Bhopal, Madhya Pradesh, India
| | - Rupal Rai
- Molecular Signalling Lab, Department of Biological Science and Engineering, Maulana Azad National Institute of Technology, Bhopal, Madhya Pradesh, India
| | - Bijina J. Mathew
- Molecular Signalling Lab, Department of Biological Science and Engineering, Maulana Azad National Institute of Technology, Bhopal, Madhya Pradesh, India
| | - Rashmi Chourasia
- Department of Chemistry, IES University, Bhopal, Madhya Pradesh, India
| | - Anirudh K. Singh
- School of Sciences, SAM Global University, Raisen, Madhya Pradesh, India
| | - Awanish Kumar
- Department of Biotechnology, National Institute of Technology, Raipur, Chhattisgarh, India
| | - Shivendra K. Chaurasiya
- Molecular Signalling Lab, Department of Biological Science and Engineering, Maulana Azad National Institute of Technology, Bhopal, Madhya Pradesh, India
- *Correspondence: Shivendra K. Chaurasiya,
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The role of Helicobacter infection on atherosclerosis in diabetic patients. Int J Diabetes Dev Ctries 2022. [DOI: 10.1007/s13410-022-01145-5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/24/2022] Open
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Kolasa-Kicińska M, Stawerska R, Stawerski P, Kałużyński A, Czkwianianc E, Lewiński A. Effects of Helicobacter pylori Infection on Ghrelin and Insulin-like Growth Factor 1 Secretion in Children with Idiopathic Short Stature. J Clin Med 2022; 11:5868. [PMID: 36233735 PMCID: PMC9572010 DOI: 10.3390/jcm11195868] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/07/2022] [Revised: 09/23/2022] [Accepted: 09/28/2022] [Indexed: 11/17/2022] Open
Abstract
BACKGROUND A diagnosis of "idiopathic short stature" (ISS) in a child means that the cause of the disease has not been established, although there are certainly some unknown factors that contributed to its occurrence. Ghrelin and leptin are important in controlling food intake; ghrelin is also a growth hormone (GH) stimulator. Both enterohormones are produced in the stomach and their secretion may be affected by a Helicobacter pylori (H. pylori) infection. METHODS Our study included a group of 61 children (53 prepubertal and 8 peripubertal) with ISS, without any gastrointestinal tract symptoms but in whom the histopathological evaluation of stomach tissue was made during gastroscopy to diagnose H. pylori infection. In each child, fasting ghrelin, leptin and IGF-1 concentrations, and GH levels in two stimulation tests were assessed. RESULTS H. pylori infection was confirmed in 24.6% of the children. Ghrelin and IGF-1 concentrations were significantly lower in H. pylori-positive than H. pylori-negative children (this was more noticeable in prepubertal subgroups), however there was not a discrepancy in regards to GH concentrations in stimulation tests, leptin levels or the nutritional state between groups. CONCLUSIONS Short children, infected by H. pylori seem to have lower ghrelin and IGF-1 concentrations than children without infection, this may be the reason for a worse growth rate in this subgroup.
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Affiliation(s)
- Marzena Kolasa-Kicińska
- Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital–Research Institute, 93-338 Lodz, Poland
| | - Renata Stawerska
- Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital–Research Institute, 93-338 Lodz, Poland
- Department of Paediatric Endocrinology, Medical University of Lodz, 93-338 Lodz, Poland
| | - Paweł Stawerski
- Consilio Diagnostyka, Laboratory of Histopathology, 93-357 Lodz, Poland
| | - Andrzej Kałużyński
- Department of Clinical Pathomorphology, Polish Mother’s Memorial Hospital–Research Institute, 93-338 Lodz, Poland
| | - Elżbieta Czkwianianc
- Department of Gastroenterology, Allergology and Paediatrics, Polish Mother’s Memorial Hospital–Research Institute, 93-338 Lodz, Poland
| | - Andrzej Lewiński
- Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital–Research Institute, 93-338 Lodz, Poland
- Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, 93-338 Lodz, Poland
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Nigatie M, Melak T, Asmelash D, Worede A. Dyslipidemia and Its Associated Factors Among Helicobacter pylori-Infected Patients Attending at University of Gondar Comprehensive Specialized Hospital, Gondar, North-West Ethiopia: A Comparative Cross-Sectional Study. J Multidiscip Healthc 2022; 15:1481-1491. [PMID: 35873092 PMCID: PMC9297042 DOI: 10.2147/jmdh.s368832] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/31/2022] [Accepted: 06/28/2022] [Indexed: 11/25/2022] Open
Abstract
Background Dyslipidemia refers to a lipid profile disturbance due to decreased high-density lipoprotein cholesterol and elevated low-density lipoprotein cholesterol, triglycerides, and total cholesterol. Helicobacter pylori infection can lead to some appetite-related disorders that may cause deregulated absorption of nutrients in the digestive system, contributing to changes in serum lipids. The purpose of this study is to assess dyslipidemia and its associated factors among H. pylori-infected patients attending at University of Gondar Comprehensive Specialized Hospital. Methods A comparative cross-sectional study was conducted on 231 H. pylori-positive and control groups, which were included by the convenience sampling technique from March to May 2021 at University of Gondar Specialized Hospital. Sociodemographic and behavioral characteristic data were collected using a pretested questionnaire, and 5mL of venous blood were used to determine the lipid profiles using DxC 700 AU chemistry analyzer. The data were analyzed using SPSS version 25. Mann–Whitney U-test and multivariable logistic regression were applied, and P-value <0.05 is considered statistically significant. Results The magnitude of dyslipidemia among H. pylori-infected patients was 71.8% (95% CI: 62.7–79.7). There was a statistically significant difference in lipid profiles between H. pylori-infected patients and control groups. The median (IQR) of lipid profiles in H. pylori-infected patients and control groups were for low-density lipoprotein: 108 (89.8, 145.5) vs 95 (79.45, 115.8, P<0.001), for triglycerides: 93 (65,117) vs 83 (58.5, 102, P=0.031), and cholesterol: 143 (119.5, 169,) vs 125 (110,143, P<0.001) mg/dl, respectively. Helicobacter pylori infection, alcohol drinking, unable to read and write, primary school, and secondary school were a significant associated variables with dyslipidemia (P<0.05). Conclusion There was a median lipid profile statistically significant difference between H. pylori-positive and control groups. Helicobacter pylori infection, educational status, and alcohol drinking habit had statistically significant association with dyslipidemia.
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Affiliation(s)
- Marye Nigatie
- Department of Medical Laboratory Science, College of medicine and Health Science, Woldia University, Woldia, Ethiopia
| | - Tadele Melak
- Department of Clinical Chemistry, School of Biomedical and Laboratory Sciences, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia
| | - Daniel Asmelash
- Department of Clinical Chemistry, School of Biomedical and Laboratory Sciences, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia
| | - Abebaw Worede
- Department of Clinical Chemistry, School of Biomedical and Laboratory Sciences, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia
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Merlotti D, Mingiano C, Valenti R, Cavati G, Calabrese M, Pirrotta F, Bianciardi S, Palazzuoli A, Gennari L. Bone Fragility in Gastrointestinal Disorders. Int J Mol Sci 2022; 23:2713. [PMID: 35269854 PMCID: PMC8910640 DOI: 10.3390/ijms23052713] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/24/2022] [Revised: 02/24/2022] [Accepted: 02/25/2022] [Indexed: 02/04/2023] Open
Abstract
Osteoporosis is a common systemic disease of the skeleton, characterized by compromised bone mass and strength, consequently leading to an increased risk of fragility fractures. In women, the disease mainly occurs due to the menopausal fall in estrogen levels, leading to an imbalance between bone resorption and bone formation and, consequently, to bone loss and bone fragility. Moreover, osteoporosis may affect men and may occur as a sequela to different diseases or even to their treatments. Despite their wide prevalence in the general population, the skeletal implications of many gastrointestinal diseases have been poorly investigated and their potential contribution to bone fragility is often underestimated in clinical practice. However, proper functioning of the gastrointestinal system appears essential for the skeleton, allowing correct absorption of calcium, vitamins, or other nutrients relevant to bone, preserving the gastrointestinal barrier function, and maintaining an optimal endocrine-metabolic balance, so that it is very likely that most chronic diseases of the gastrointestinal tract, and even gastrointestinal dysbiosis, may have profound implications for bone health. In this manuscript, we provide an updated and critical revision of the role of major gastrointestinal disorders in the pathogenesis of osteoporosis and fragility fractures.
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Affiliation(s)
- Daniela Merlotti
- Department of Medical Sciences, Azienda Ospedaliera Universitaria Senese, 53100 Siena, Italy
| | - Christian Mingiano
- Department of Medicine Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; (C.M.); (G.C.); (M.C.); (F.P.); (S.B.)
| | - Roberto Valenti
- Deparment of Surgery, Perioperative Medicine Unit, Azienda Ospedaliera Universitaria Senese, 53100 Siena, Italy;
| | - Guido Cavati
- Department of Medicine Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; (C.M.); (G.C.); (M.C.); (F.P.); (S.B.)
| | - Marco Calabrese
- Department of Medicine Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; (C.M.); (G.C.); (M.C.); (F.P.); (S.B.)
| | - Filippo Pirrotta
- Department of Medicine Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; (C.M.); (G.C.); (M.C.); (F.P.); (S.B.)
| | - Simone Bianciardi
- Department of Medicine Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; (C.M.); (G.C.); (M.C.); (F.P.); (S.B.)
| | - Alberto Palazzuoli
- Cardiovascular Disease Unit, Division of Cardiology, Department of Medical Biotechnologies, Azienda Ospedaliera Universitaria Senese, 53100 Siena, Italy;
| | - Luigi Gennari
- Department of Medicine Surgery and Neuroscience, University of Siena, 53100 Siena, Italy; (C.M.); (G.C.); (M.C.); (F.P.); (S.B.)
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11
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Shinozaki S, Osawa H, Hayashi Y, Miura Y, Yano T, Lefor AK, Yamamoto H. Predictors and timing for the development of symptomatic gastroesophageal reflux disease after successful Helicobactor pylori eradication therapy. Scand J Gastroenterol 2022; 57:16-21. [PMID: 34547219 DOI: 10.1080/00365521.2021.1975310] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
BACKGROUND Helicobacter pylori (H. pylori) eradication success increases the incidence of erosive esophagitis by normalization of gastric acid secretion. The aim of this study is to clarify predictors and timing for the development of symptomatic gastroesophageal reflux disease (GERD) after successful H. pylori eradication based on long-term follow-up. METHODS From April 2014 to October 2020, 330 patients with H. pylori infections treated with a standard triple-drug regimen were enrolled, and their records retrospectively reviewed. Development of symptomatic GERD was defined as requiring proton pump inhibitor or vonoprazan therapy to treat symptoms. RESULTS The mean follow-up period was 2.8 years, and symptomatic GERD developed in 41 (12%) patients during the study period. Overall rates of GERD-symptom free patients at 6 months, 1, and 2 years after eradication were 97%, 93%, and 89%, respectively. We evaluated predictors for the development of symptomatic GERD using a Cox proportional hazards regression model. In multivariate analysis, being a current smoker, having functional dyspepsia, hiatal hernia, and severe gastric atrophy were identified as significant predictive factors. The GERD domain score in the Izumo scale was significantly decreased 1 month after vonoprazan therapy consistent with effective treatment of symptomatic GERD. CONCLUSIONS The rate of development of symptomatic GERD after successful H. pylori eradication is low over long-term follow-up and is easily controlled by vonoprazan therapy. However, patients with smoking habits, functional dyspepsia, hiatal hernia, or severe gastric atrophy should be followed carefully after eradication.
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Affiliation(s)
- Satoshi Shinozaki
- Shinozaki Medical Clinic, Utsunomiya, Japan.,Department of Medicine, Division of Gastroenterology, Jichi Medical University, Shimotsuke, Japan
| | - Hiroyuki Osawa
- Department of Medicine, Division of Gastroenterology, Jichi Medical University, Shimotsuke, Japan
| | - Yoshikazu Hayashi
- Department of Medicine, Division of Gastroenterology, Jichi Medical University, Shimotsuke, Japan
| | - Yoshimasa Miura
- Department of Medicine, Division of Gastroenterology, Jichi Medical University, Shimotsuke, Japan
| | - Tomonori Yano
- Department of Medicine, Division of Gastroenterology, Jichi Medical University, Shimotsuke, Japan
| | | | - Hironori Yamamoto
- Department of Medicine, Division of Gastroenterology, Jichi Medical University, Shimotsuke, Japan
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12
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Yücel O. GER and Helicobacter pylori. GASTROESOPHAGEAL REFLUX IN CHILDREN 2022:167-188. [DOI: 10.1007/978-3-030-99067-1_14] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/03/2025]
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13
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Azami M, Baradaran HR, Dehghanbanadaki H, Kohnepoushi P, Saed L, Moradkhani A, Moradpour F, Moradi Y. Association of Helicobacter pylori infection with the risk of metabolic syndrome and insulin resistance: an updated systematic review and meta-analysis. Diabetol Metab Syndr 2021; 13:145. [PMID: 34922625 PMCID: PMC8684139 DOI: 10.1186/s13098-021-00765-x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/06/2021] [Accepted: 11/30/2021] [Indexed: 12/16/2022] Open
Abstract
BACKGROUND Conflicting results of recent studies on the association between Helicobacter pylori (H. pylori) infection and the risk of insulin resistance and metabolic syndrome explored the need for updated meta-analysis on this issue. Therefore, this systematic review aimed to estimate the pooled effect of H. pylori infection on the risk of insulin resistance and metabolic syndrome. METHODS To identify case-control studies and cohort studies evaluating the association of H. pylori infection with insulin resistance and metabolic syndrome, a comprehensive literature search was performed from international databases including Medline (PubMed), Web of Sciences, Scopus, EMBASE, and CINHAL from January 1990 until January 2021. We used odds ratio with its 95% confidence interval to quantify the effect of case-control studies and risk ratio with its 95% CI for the effect of cohort studies. RESULTS 22 studies with 206,911 participants were included for meta-analysis. The pooled estimate of odds ratio between H. pylori infection and metabolic syndrome in case-control studies was 1.19 (95% CI 1.05-1.35; I2 = 0%), and in cohort studies, the pooled risk ratio was 1.31 (95% CI 1.13-1.51; I2 = 0%). Besides, case-control studies showed the pooled odds ratio of 1.54 (95% CI 1.19-1.98; I2 = 6.88%) for the association between H. pylori infection and insulin resistance. CONCLUSION In this meta-analysis, the results showed that there was a possibility of metabolic syndrome and insulin resistance in case of H. pylori infection.
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Affiliation(s)
- Mobin Azami
- Student Research Committee, Kurdistan University of Medical Sciences, Sanandaj, Iran
| | - Hamid Reza Baradaran
- Ageing Clinical & Experimental Research Team, Institute of Applied Health Sciences, University of Aberdeen, Aberdeen, UK
- Endocrine Research Center, Institute of Endocrinology and Metabolism, Iran University of Medical Sciences, Sanandaj, Iran
| | - Hojat Dehghanbanadaki
- Students Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran
| | - Parisa Kohnepoushi
- Student Research Committee, Kurdistan University of Medical Sciences, Sanandaj, Iran
| | - Lotfolah Saed
- Department of Endocrinology, Faculty of Medicine, Kurdistan University of Medical Science, Sanandaj, Iran
| | - Asra Moradkhani
- Student Research Committee, Kurdistan University of Medical Sciences, Sanandaj, Iran
| | - Farhad Moradpour
- Social Determinants of Health Research Center, Research Institute for Health Development, Kurdistan University of Medical Science, Sanandaj, Iran
| | - Yousef Moradi
- Social Determinants of Health Research Center, Research Institute for Health Development, Kurdistan University of Medical Science, Sanandaj, Iran
- Department of Biostatics and Epidemiology, Faculty of Medicine, Kurdistan University of Medical Science, Sanandaj, Iran
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14
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Lewiński A, Karbownik-Lewińska M, Wieczorek-Szukała K, Stasiak M, Stawerska R. Contribution of Ghrelin to the Pathogenesis of Growth Hormone Deficiency. Int J Mol Sci 2021; 22:9066. [PMID: 34445772 PMCID: PMC8396656 DOI: 10.3390/ijms22169066] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/22/2021] [Revised: 08/17/2021] [Accepted: 08/20/2021] [Indexed: 02/07/2023] Open
Abstract
In this review we described the interactions between ghrelin and the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis in children and adults with growth hormone deficiency (GHD). A possible involvement of these interactions in the pathogenesis of unexplained cases of GHD was suggested. Current research provides more and more details to the knowledge on the circadian rhythm of ghrelin. We gathered reports on the decreasing effect of Helicobacter pylori-related chronic gastritis on the number of ghrelin immunopositive cells and the consequent decrease in ghrelin serum concentration. The gastrointestinal tract microflora modification of the ghrelin action, by the mechanism of molecular mimicry, was also stressed. Moreover, the mutual relationships between ghrelin and the TSH-FT4/FT3 axis in growth and metabolic processes are described. It is to be recalled that FT4 and FT3 exert a permissive impact on IGF-1 action and, in turn, GH, in reaction mediated by IGF-1, enhances the monodeiodination of FT4 to FT3. Finally, we discussed the latest attempts to use the GH secretagogue receptor (GHS-R) analogues for possible diagnostic and therapeutic purposes.
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Affiliation(s)
- Andrzej Lewiński
- Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, 93-338 Lodz, Poland;
- Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital—Research Institute, 93-338 Lodz, Poland; (M.K.-L.); (M.S.); (R.S.)
| | - Małgorzata Karbownik-Lewińska
- Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital—Research Institute, 93-338 Lodz, Poland; (M.K.-L.); (M.S.); (R.S.)
- Department of Oncological Endocrinology, Medical University of Lodz, 90-419 Lodz, Poland
| | | | - Magdalena Stasiak
- Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital—Research Institute, 93-338 Lodz, Poland; (M.K.-L.); (M.S.); (R.S.)
| | - Renata Stawerska
- Department of Endocrinology and Metabolic Diseases, Polish Mother’s Memorial Hospital—Research Institute, 93-338 Lodz, Poland; (M.K.-L.); (M.S.); (R.S.)
- Department of Paediatric Endocrinology, Medical University of Lodz, 90-419 Lodz, Poland
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15
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Spiridon IA, Ciobanu DGA, Giușcă SE, Căruntu ID. Ghrelin and its role in gastrointestinal tract tumors (Review). Mol Med Rep 2021; 24:663. [PMID: 34296307 PMCID: PMC8335721 DOI: 10.3892/mmr.2021.12302] [Citation(s) in RCA: 12] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2021] [Accepted: 06/23/2021] [Indexed: 12/13/2022] Open
Abstract
Ghrelin, an orexigenic hormone, is a peptide that binds to the growth hormone secretagogue receptor; it is secreted mainly by enteroendocrine cells in the oxyntic glands of the stomach. Ghrelin serves a role in both local and systemic physiological processes, and is implicated in various pathologies, including neoplasia, with tissue expression in several types of malignancies in both in vitro and in vivo studies. However, the precise implications of the ghrelin axis in metastasis, invasion and cancer progression regulation has yet to be established. In the case of gastrointestinal (GI) tract malignancies, ghrelin has shown potential to become a prognostic factor or even a therapeutic target, although data in the literature are inconsistent and unsystematic, with reports untailored to a specific histological subtype of cancer or a particular localization. The evaluation of immunohistochemical expression shows a limited outlook owing to the low number of cases analyzed, and in vivo analyses have conflicting data regarding differences in ghrelin serum levels in patients with cancer. The aim of this review was to examine the relationship between ghrelin and GI tract malignancies to demonstrate the inconsistencies in current results and to highlight its clinical significance in the outcome of these patients.
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Affiliation(s)
- Irene Alexandra Spiridon
- Department of Pathology, 'Grigore T. Popa' University of Medicine and Pharmacy, Iași 700115, Romania
| | | | - Simona Eliza Giușcă
- Department of Pathology, 'Grigore T. Popa' University of Medicine and Pharmacy, Iași 700115, Romania
| | - Irina Draga Căruntu
- Department of Histology, 'Grigore T. Popa' University of Medicine and Pharmacy, Iași 700115, Romania
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16
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Baradaran A, Dehghanbanadaki H, Naderpour S, Pirkashani LM, Rajabi A, Rashti R, Riahifar S, Moradi Y. The association between Helicobacter pylori and obesity: a systematic review and meta-analysis of case-control studies. Clin Diabetes Endocrinol 2021; 7:15. [PMID: 34243821 PMCID: PMC8272347 DOI: 10.1186/s40842-021-00131-w] [Citation(s) in RCA: 19] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/04/2021] [Accepted: 06/16/2021] [Indexed: 12/20/2022] Open
Abstract
INTRODUCTION The relationship between H. pylori infection and obesity development has remained controversial among various studies. The aim of this study was to clarify the pooled effect of H. pylori infection on the development of obesity and vice versa. METHODS We searched international databases including Medline (PubMed), Web of sciences, Scopus, EMBASE, Cochrane, Ovid, and CINHAL to retrieve all case-control studies reporting the effect of H. pylori on obesity and vice versa, which had been published in English between January 1990 and June 2019. The quality of included studies was assessed by the Modified Newcastle-Ottawa Scale for Case-Control studies. The logarithm of the odds ratio (OR) and its standard error was used for the meta-analysis. RESULTS Eight case-control studies with 25,519 participants were included for qualitative and quantitative analyses. The pooled analysis showed that obese participants had a higher risk of H. pylori infection than lean participants with an odds ratio of 1.46 (95%CI: 1.26, 1.68). Also, the pooled analysis revealed that participants infected by H. pylori had a higher risk of obesity than non-infected participants with an odds ratio of 1.01 (95%CI: 1.01, 1.02). CONCLUSION The results of this meta-analysis showed that there was a positive correlation between the risk of H. pylori infection and the prevalence of obesity development. Thus, H. pylori positive patients were more likely to be obese, and obese individuals had higher risks of H. pylori infection.
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Affiliation(s)
- Ali Baradaran
- Endocrine Research Center, Institute of Endocrinology and Metabolism, Iran University of Medical Sciences, Tehran, Iran
| | - Hojat Dehghanbanadaki
- Students Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran
| | - Sara Naderpour
- Department of Epidemiology, School of Public Health, Iran University of Medical Sciences, Tehran, Iran
| | - Leila Mohammadi Pirkashani
- Clinical Research Development Center, Imam Reza Hospital, Kermanshah University of Medical Sciences, Kermanshah, Iran
| | - Abdolhalim Rajabi
- Department of Health Management and Social Development Research Center, Faculty of Health, Golestan University of Medical Sciences, Gorgan, Iran
| | - Roya Rashti
- Social Determinants of Health Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, 66179-13446 Iran
| | - Sevda Riahifar
- Department of Biostatistics, Faculty of Public Health, Iran University of Medical Sciences, Tehran, Iran
| | - Yousef Moradi
- Social Determinants of Health Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, 66179-13446 Iran
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17
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Zheng J, Cai W, Lu X, He W, Li D, Zhong H, Yang L, Li S, Li H, Rafee S, Zhao Z, Wang Q, Pan H. Chronic stress accelerates the process of gastric precancerous lesions in rats. J Cancer 2021; 12:4121-4133. [PMID: 34093815 PMCID: PMC8176425 DOI: 10.7150/jca.52658] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/31/2020] [Accepted: 04/23/2021] [Indexed: 02/06/2023] Open
Abstract
Background: Gastrointestinal cancers account for 20% of all deaths worldwide. Gastric cancer (GC) patients are susceptible to psychological change, especially depression which is commonly induced by chronic stress. Gastric precancerous lesions (GPL) is an important prodromal stage in the occurrence of gastric cancer. Chronic stress influences the prognosis of GC and may influence the process of GPL as well. Methods: Sixty SD rats were randomly divided into a control group, GPL group, and GPL+CUMS group. In the GPL group, 200μg/mL N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) free drinking method combined with intermittent fasting was applied to establish the GPL animal model. Based on this, we combined the GPL rats with chronic unpredicted mild stress (CUMS) to establish a comprehensive model. We then evaluated their behavior by open field tests and sucrose preference tests. We tested the IL-6, IL-10, TNF-α, Ghrelin, Leptin and Somatostatin (SS) levels in serum and observed the expression of Ghrelin and Gastrokine 2(GKN2) in the gastric mucosa of rats with tumors by immunofluorescence. Results: Our results showed that GPL and GPL+CUMS rats all displayed a significantly decreased total distance and mean velocity traveled in the open field test. The percentages of sucrose preference were significantly decreased in the GPL+CUMS group compared to the control group. In addition, IL-6 and TNF-α were significantly increased in both the GPL and GPL+CUMS groups. Furthermore, the GPL+CUMS group showed significantly increased TNF-α levels in serum compared to the GPL rats. Our results showed that the expression of NF-κB, p53, and BCL-2 were significantly increased while BAX was reduced in the GPL and GPL+CUMS groups. Moreover, Ghrelin and Leptin levels in serum were significantly decreased in the GPL and GPL+CUMS groups. SS levels in serum were significantly increased in the GPL+CUMS group. Additionally, we found that the GPL+CUMS rats with tumors not only had strong expression of GKN2 on the luminal side and the lamina propria of the gastric mucosa and tumor, but also had expression of Ghrelin on the luminal side of the gastric mucosa. The areas that showed strong expression of GKN2 and Ghrelin, are all located around the blood vessels in the tumor. Conclusions: GPL rats under chronic stress would aggravate the conditions of GPL, shorten the process of GPL, and increase the risk of tumorigenesis. In addition, the close monitoring of the mental health of cancer survivors and precancerous lesion patients is suggested to be of great significance in the prevention and treatment of cancer.
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Affiliation(s)
- Jiayi Zheng
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Institute of Gastroenterology, Guangzhou University of Chinese Medicine, China
| | - Weiwu Cai
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, China
| | - Xuen Lu
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Clinical Medical College of Acupuncture Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, China
| | - Wei He
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, China
| | - Ding Li
- The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China
| | - Haoyu Zhong
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Clinical Medical College of Acupuncture Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, China
| | - Liangjun Yang
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Institute of Gastroenterology, Guangzhou University of Chinese Medicine, China
| | - Siyi Li
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, China
| | - Haishan Li
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Second Clinical Medical College of Guangzhou university of Chinese Medicine
| | - Sereen Rafee
- Rutgers University Graduate School of Biomedical Sciences, Newark, NJ, USA
| | - Ziming Zhao
- Guangdong Province Engineering Technology Research Institute of Traditional Chinese Medicine, Guangzhou, China
| | - Qi Wang
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, China
| | - Huafeng Pan
- Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.,Institute of Gastroenterology, Guangzhou University of Chinese Medicine, China.,Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, Guangzhou, China
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18
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Mathus-Vliegen E, Spångeus A, Walter S, Ericson AC. Weight loss with or without intragastric balloon causes divergent effects on ghrelin cell expression. Obes Sci Pract 2021; 7:199-207. [PMID: 33841889 PMCID: PMC8019283 DOI: 10.1002/osp4.478] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/20/2020] [Revised: 12/03/2020] [Accepted: 12/09/2020] [Indexed: 12/11/2022] Open
Abstract
Objective The mechanism of action of intragastric balloons in the treatment of obesity is not fully understood. One of the hypotheses is that balloons might have an effect on the fundus, the area of ghrelin production. Methods Participants were randomized to a 13‐week period of sham or balloon treatment followed by a 13‐week period of balloon therapy in everyone. Blood samples for ghrelin levels were taken in the fasting state and after a breakfast at the start, after 13 and 26 weeks. Biopsies for ghrelin cell immunohistochemistry were taken from the fundus at endoscopy. Results Seven participants entered the balloon–balloon (BB) group and 11 the sham–balloon (SB) group. Despite a considerable weight loss, a median −17.9 kg (interquartile ranges −23.8 to −0.5) in the BB group and −18.3 kg (−22.7 to −14.7) in the SB group, fasting ghrelin and meal‐induced ghrelin response did not change. In the SB group, the number of ghrelin cells increased significantly (p 0.001) from 110.6 (83.6–118.9) to 160.2 (128.5–223.0) while on sham treatment and returned to initial levels, 116.3 (91.7–146.9) (p 0.001), when they received their first balloon. No significant changes in ghrelin cell numbers were observed in the BB group. Conclusion In participants without a balloon, weight loss induced an increase in ghrelin cell numbers in the fundus, which was annulled by the subsequent placement of a balloon. The effect of a balloon might be explained by effects on ghrelin cell numbers or ghrelin cell activity.
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Affiliation(s)
- Elisabeth Mathus-Vliegen
- Department of Gastroenterology and Hepatology Academic Medical Centre (AMC) University of Amsterdam Amsterdam the Netherlands
| | - Anna Spångeus
- Department of Health, Medicine and Caring Sciences Division of Diagnostics and Specialist Medicine Linköping University Linköping Sweden.,Department of Acute Internal Medicine and Geriatrics Linköping University Hospital Linköping University Linköping Sweden
| | - Susanna Walter
- Department of Biomedical and Clinical Sciences Division of Inflammation and Infection Medical Faculty Linköping University Linköping Sweden.,Department of Gastroenterology Linköping University Hospital Linköping University Linköping Sweden
| | - Ann-Charlott Ericson
- Department of Biomedical and Clinical Sciences Division of Molecular Medicine and Virology Medical Faculty Linköping University Linköping Sweden
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19
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Chen CC, Liou JM, Lee YC, Hong TC, El-Omar EM, Wu MS. The interplay between Helicobacter pylori and gastrointestinal microbiota. Gut Microbes 2021; 13:1-22. [PMID: 33938378 PMCID: PMC8096336 DOI: 10.1080/19490976.2021.1909459] [Citation(s) in RCA: 90] [Impact Index Per Article: 22.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/02/2020] [Revised: 03/10/2021] [Accepted: 03/19/2021] [Indexed: 02/07/2023] Open
Abstract
The complex population of microbes in the human gastrointestinal (GI) tract interacts with itself and with the host, exerting a deep influence on health and disease development. The development of modern sequencing technology has enabled us to gain insight into GI microbes. Helicobacter pylori colonization significantly affects the gastric microenvironment, which in turn affects gastric microbiota and may be correlated with colonic microbiota changes. Crosstalk between H. pylori and GI commensal flora may play a role in H. pylori-related carcinogenicity and extragastric manifestations. We review current knowledge on how H. pylori shapes GI microbiota with a specific focus on its impact on the stomach and colon. We also review current evidence on colonic microbiota changes attributed to eradication therapy based on the clinical studies performed to date.
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Affiliation(s)
- Chieh-Chang Chen
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
- Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
- Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Jyh-Ming Liou
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
- Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
- Department of Medicine, National Taiwan University Cancer Center, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Yi-Chia Lee
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
- Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
- Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan
| | - Tzu-Chan Hong
- Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
| | - Emad M El-Omar
- Microbiome Research Centre, St George & Sutherland Clinical School, University of New South Wales, Sydney, NSW, Australia
| | - Ming-Shiang Wu
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
- Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
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20
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Gennari L, Merlotti D, Figura N, Mingiano C, Franci MB, Lucani B, Picchioni T, Alessandri M, Campagna MS, Gonnelli S, Bianciardi S, Materozzi M, Caffarelli C, Gonnelli S, Nuti R. Infection by CagA-Positive Helicobacter pylori Strains and Bone Fragility: A Prospective Cohort Study. J Bone Miner Res 2021; 36:80-89. [PMID: 32790186 DOI: 10.1002/jbmr.4162] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/25/2020] [Revised: 07/31/2020] [Accepted: 08/05/2020] [Indexed: 02/06/2023]
Abstract
Helicobacter pylori (HP) infection is a common and persistent disorder acting as a major cofactor for the development of upper gastrointestinal diseases and several extraintestinal disorders including osteoporosis. However, no prospective study assessed the effects of HP on bone health and fracture risk. We performed a HP screening in a population-based cohort of 1149 adults followed prospectively for up to 11 years. The presence of HP infection was assessed by serologic testing for serum antibodies to HP and the cytotoxin associated gene-A (CagA). The prevalence of HP infection did not differ among individuals with normal bone mineral density (BMD), osteoporosis, and osteopenia. However, HP infection by CagA-positive strains was significantly increased in osteoporotic (30%) and osteopenic (26%) patients respect to subjects with normal BMD (21%). Moreover, anti-CagA antibody levels were significantly and negatively associated with lumbar and femoral BMD. Consistent with these associations, patients affected by CagA-positive strains had a more than fivefold increased risk to sustain a clinical vertebral fracture (HR 5.27; 95% CI, 2.23-12.63; p < .0001) and a double risk to sustain a nonvertebral incident fracture (HR 2.09; 95% CI, 1.27-2.46; p < .005). Reduced estrogen and ghrelin levels, together with an impaired bone turnover balance after the meal were also observed in carriers of CagA-positive HP infection. HP infection by strains expressing CagA may be considered a risk factor for osteoporosis and fractures. Further studies are required to clarify in more detail the underlying pathogenetic mechanisms of this association. © 2020 American Society for Bone and Mineral Research (ASBMR).
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Affiliation(s)
- Luigi Gennari
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Daniela Merlotti
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Natale Figura
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Christian Mingiano
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Maria Beatrice Franci
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Barbara Lucani
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Tommaso Picchioni
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Mario Alessandri
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Maria Stella Campagna
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Sara Gonnelli
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Simone Bianciardi
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Maria Materozzi
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy.,Department of Medical Biotechnologies, University of Siena, Siena, Italy
| | - Carla Caffarelli
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Stefano Gonnelli
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
| | - Ranuccio Nuti
- Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy
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21
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Liou JM, Malfertheiner P, Lee YC, Sheu BS, Sugano K, Cheng HC, Yeoh KG, Hsu PI, Goh KL, Mahachai V, Gotoda T, Chang WL, Chen MJ, Chiang TH, Chen CC, Wu CY, Leow AHR, Wu JY, Wu DC, Hong TC, Lu H, Yamaoka Y, Megraud F, Chan FKL, Sung JJ, Lin JT, Graham DY, Wu MS, El-Omar EM. Screening and eradication of Helicobacter pylori for gastric cancer prevention: the Taipei global consensus. Gut 2020; 69:2093-2112. [PMID: 33004546 DOI: 10.1136/gutjnl-2020-322368] [Citation(s) in RCA: 275] [Impact Index Per Article: 55.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/28/2020] [Revised: 07/27/2020] [Accepted: 08/12/2020] [Indexed: 02/06/2023]
Abstract
OBJECTIVE A global consensus meeting was held to review current evidence and knowledge gaps and propose collaborative studies on population-wide screening and eradication of Helicobacter pylori for prevention of gastric cancer (GC). METHODS 28 experts from 11 countries reviewed the evidence and modified the statements using the Delphi method, with consensus level predefined as ≥80% of agreement on each statement. The Grading of Recommendation Assessment, Development and Evaluation (GRADE) approach was followed. RESULTS Consensus was reached in 26 statements. At an individual level, eradication of H. pylori reduces the risk of GC in asymptomatic subjects and is recommended unless there are competing considerations. In cohorts of vulnerable subjects (eg, first-degree relatives of patients with GC), a screen-and-treat strategy is also beneficial. H. pylori eradication in patients with early GC after curative endoscopic resection reduces the risk of metachronous cancer and calls for a re-examination on the hypothesis of 'the point of no return'. At the general population level, the strategy of screen-and-treat for H. pylori infection is most cost-effective in young adults in regions with a high incidence of GC and is recommended preferably before the development of atrophic gastritis and intestinal metaplasia. However, such a strategy may still be effective in people aged over 50, and may be integrated or included into national healthcare priorities, such as colorectal cancer screening programmes, to optimise the resources. Reliable locally effective regimens based on the principles of antibiotic stewardship are recommended. Subjects at higher risk of GC, such as those with advanced gastric atrophy or intestinal metaplasia, should receive surveillance endoscopy after eradication of H. pylori. CONCLUSION Evidence supports the proposal that eradication therapy should be offered to all individuals infected with H. pylori. Vulnerable subjects should be tested, and treated if the test is positive. Mass screening and eradication of H. pylori should be considered in populations at higher risk of GC.
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Affiliation(s)
- Jyh-Ming Liou
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.,Department of Medicine, National Taiwan University Cancer Center, Taipei, Taiwan
| | - Peter Malfertheiner
- Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.,Department of Medicine II, University Hospital, LMU Munich, Munich, Germany
| | - Yi-Chia Lee
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.,Department of Medical Research, National Taiwan University Hospital, Taipei, Taiwan
| | - Bor-Shyang Sheu
- Department of Internal Medicine and Institute of Clinical Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.,Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
| | - Kentaro Sugano
- Department of Medicine, Jichi Medical School, Tochigi, Japan
| | - Hsiu-Chi Cheng
- Department of Internal Medicine and Institute of Clinical Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.,Department of Internal Medicine, Tainan Hospital, Ministry of Health and Welfare, Tainan, Taiwan
| | - Khay-Guan Yeoh
- Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
| | - Ping-I Hsu
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, An Nan Hospital, China Medical University, Tainan, Taiwan
| | - Khean-Lee Goh
- Department of Gastroenterology and Hepatology, University of Malaya, Kuala Lumpur, Malaysia
| | - Varocha Mahachai
- Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Bangkok, Thailand
| | - Takuji Gotoda
- Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
| | - Wei-Lun Chang
- Department of Internal Medicine and Institute of Clinical Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
| | - Mei-Jyh Chen
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.,Integrated Diagnostics and Therapeutics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Tsung-Hsien Chiang
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.,Integrated Diagnostics and Therapeutics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Chieh-Chang Chen
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Chun-Ying Wu
- Institute of Biomedical Informatics, School of Medicine, National Yang-Ming University, Taipei, Taiwan.,Division of Translational Research, Department of Medical Research, Taipei Veterans General Hospital, Taipei, Taiwan
| | - Alex Hwong-Ruey Leow
- Department of Gastroenterology and Hepatology, University of Malaya, Kuala Lumpur, Malaysia
| | - Jeng-Yih Wu
- Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
| | - Deng-Chyang Wu
- Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
| | - Tzu-Chan Hong
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University Hospital Bei-Hu Branch, Taipei, Taiwan
| | - Hong Lu
- Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
| | - Yoshio Yamaoka
- Oita University Faculty of Medicine, Yufu, Oita, Japan.,Department of Medicine, Michael E DeBakey VA Medical Center and Baylor College of Medicine, Houston, Texas, USA
| | - Francis Megraud
- French National Reference Centre for Helicobacters, Bacteriology laboratory, Pellegrin Hospital, Bordeaux, & INSERM U1053, University of Bordeaux, Bordeaux, France
| | - Francis K L Chan
- Institute of Digestive Disease, Chinese University of Hong Kong, Shatin, Hong Kong, China.,Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong, China
| | - Joseph Jy Sung
- Institute of Digestive Disease, Chinese University of Hong Kong, Shatin, Hong Kong, China.,Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong, China
| | - Jaw-Town Lin
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.,Digestive Medicine Center, China Medical University Hospital, Taichung, Taiwan
| | - David Y Graham
- Department of Medicine, Michael E DeBakey VA Medical Center and Baylor College of Medicine, Houston, Texas, USA
| | - Ming-Shiang Wu
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan .,Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Emad M El-Omar
- Department of Medicine, University of New South Wales, Sydney, New South Wales, Australia.,Microbiome Research Centre, St George & Sutherland Clinical School, University of New South Wales, Sydney, NSW, Australia
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22
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Chen X, Zhang J, Wang R, Liu H, Bao C, Wu S, Wen J, Yang T, Wei Y, Ren S, Tong Y, Zhao Y. UPLC-Q-TOF/MS-Based Serum and Urine Metabonomics Study on the Ameliorative Effects of Palmatine on Helicobacter pylori-Induced Chronic Atrophic Gastritis. Front Pharmacol 2020; 11:586954. [PMID: 33041831 PMCID: PMC7522567 DOI: 10.3389/fphar.2020.586954] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/24/2020] [Accepted: 08/27/2020] [Indexed: 12/15/2022] Open
Abstract
Objective The main objective of this study was to investigate the ameliorative effects of Palmatine (Pal) on Helicobacter pylori (H. pylori) induced chronic atrophic gastritis (CAG) Method Body function, serum biochemical indicators and histopathology were used to evaluate the pharmacodynamics of Pal on CAG rats. The target genes expression levels were verified and assessed by RT-PCR and immunohistochemistry (IHC). Moreover, UPLC-Q-TOF/MS analysis based on urine and serum was performed to identify the potential metabolites in the pathological process of CAG induced by H. pylori. Metabolic pathway analysis was performed to elucidate the metabolic network associated with Pal treatment of CAG. Results Pal (10, 20, 40 mg/kg/day) significantly restored the body function of CAG rats, reduced the serum biochemical indicators, and maintained the integrity of the gastric mucosal epithelial barrier while alleviated gastric histological damage. Metabolomics analysis shows that the therapeutic effect of Pal on CAG involves 10 metabolites and 10 metabolic pathways, of which the Taurine and hypotaurine metabolism, Glycerophospholipid metabolism and Pentose and glucuronate interconversions are closely related to the gastrointestinal protection of Pal, and these metabolic pathways crosstalk with each other due to the internet hub of citric acid cycle. Conclusions Metabolomics was used for the first time to identify potential biomarkers of CAG and to illuminate the therapeutic mechanism of Pal on CAG induced by H. pylori. The results provided a new insight for further research on CAG treatment.
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Affiliation(s)
- Xing Chen
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China.,College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Jianzhong Zhang
- Center of Disease Control and Prevention, National Institute for Communicable Disease Control and Prevention, Beijing, China
| | - Ruilin Wang
- Integrative Medical Center, Fifth Medical Center of PLA General Hospital, Beijing, China
| | - Honghong Liu
- Integrative Medical Center, Fifth Medical Center of PLA General Hospital, Beijing, China
| | - Chunmei Bao
- Division of Clinical Microbiology, Fifth Medical Center of PLA General Hospital, Beijing, China
| | - Shihua Wu
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China.,College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Jianxia Wen
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China.,College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Tao Yang
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China.,College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Ying Wei
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China.,College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Sichen Ren
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China.,College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Yuling Tong
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China.,College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Yanling Zhao
- Department of Pharmacy, Fifth Medical Center of PLA General Hospital, Beijing, China
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23
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Shimamoto T, Yamamichi N, Gondo K, Takahashi Y, Takeuchi C, Wada R, Mitsushima T, Koike K. The association of Helicobacter pylori infection with serum lipid profiles: An evaluation based on a combination of meta-analysis and a propensity score-based observational approach. PLoS One 2020; 15:e0234433. [PMID: 32511269 PMCID: PMC7279579 DOI: 10.1371/journal.pone.0234433] [Citation(s) in RCA: 21] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/07/2020] [Accepted: 05/25/2020] [Indexed: 12/14/2022] Open
Abstract
Background Several previous studies have suggested that Helicobacter pylori (H. pylori) infection affects the serum lipid profile. However, it remains controversial and the mechanism has not been elucidated. The purpose of this study is to use an epidemiological perspective to evaluate the association between H. pylori infection and the serum lipid profile. Methods Multivariate analysis was performed using the data of serum lipid profile, infection status of H. pylori, fitness/lifestyle habits, and various subjects’ characteristics which were derived from the 15,679 generally healthy individuals in Japan. The average treatment effects (ATEs) of H. pylori infection on the serum lipid profile were estimated using augmented inverse probability weighting (AIPW). A meta-analysis was also performed using the 27 studies worldwide in which the status of H. pylori infection and at least one serum examination value (high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), or triglyceride (TG)) were described. Results The ATEs determined with AIPW showed that H. pylori infection has significant positive effects on LDL-C and TC (ATE (95% confidence interval [95%CI]) = 3.4 (2.36–4.49) and 1.7 (0.58–2.88), respectively) but has significant negative effects on HDL-C and TG (ATE (95%CI) = −1.2 (−1.74 to −0.72) and −3.5 (−5.92 to −1.06), respectively). The meta-analysis to estimate the association between H. pylori infection and the serum lipid profile revealed that H. pylori infection is positively associated with LDL-C, TC, and TG (standardized mean difference [SMD] (95%CI) = 0.11 (0.09–0.12), 0.09 (0.07–0.10) and 0.06 (0.05–0.08), respectively) and negatively associated with HDL-C (SMD = −0.13 (−0.14 to −0.12)). Conclusion Both our multivariate analyses and meta-analysis showed that H. pylori infection significantly affects the serum lipid profile, which might lead to various dyslipidemia-induced severe diseases like coronary thrombosis or cerebral infarction.
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Affiliation(s)
- Takeshi Shimamoto
- Department of Medical Statistics and Information, Kameda Medical Center Makuhari, Mihama-ku, Chiba, Japan
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan
| | - Nobutake Yamamichi
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan
- * E-mail:
| | - Kenta Gondo
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan
| | - Yu Takahashi
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan
| | - Chihiro Takeuchi
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan
| | - Ryoichi Wada
- Department of Medical Statistics and Information, Kameda Medical Center Makuhari, Mihama-ku, Chiba, Japan
| | - Toru Mitsushima
- Department of Medical Statistics and Information, Kameda Medical Center Makuhari, Mihama-ku, Chiba, Japan
| | - Kazuhiko Koike
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan
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24
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Hirabayashi M, Inoue M, Sawada N, Saito E, Abe SK, Hidaka A, Iwasaki M, Yamaji T, Shimazu T, Shibuya K, Tsugane S. Effect of body-mass index on the risk of gastric cancer: A population-based cohort study in A Japanese population. Cancer Epidemiol 2019; 63:101622. [DOI: 10.1016/j.canep.2019.101622] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/20/2019] [Revised: 09/30/2019] [Accepted: 10/04/2019] [Indexed: 12/24/2022]
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25
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Xu X, Li W, Qin L, Yang W, Yu G, Wei Q. Relationship between Helicobacter pylori infection and obesity in Chinese adults: A systematic review with meta-analysis. PLoS One 2019; 14:e0221076. [PMID: 31509542 PMCID: PMC6738918 DOI: 10.1371/journal.pone.0221076] [Citation(s) in RCA: 40] [Impact Index Per Article: 6.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/02/2019] [Accepted: 07/30/2019] [Indexed: 12/15/2022] Open
Abstract
BACKGROUND Obesity is highly prevalent worldwide. More and more studies have been conducted on the relationship between H. pylori infection and obesity or overweight. But the relationship between them is controversial in the literatures and there is no comprehensive evidence for the correlation. AIM To evaluate the prevalence of H. pylori infection in Chinese adult subjects who received routine physical examinations and the relationship between H. pylori and obesity. METHODS Literatures on H. pylori infection and obesity in Chinese population were searched in online databases. Relevant data were extracted independently by two researchers and meta-analysis was performed by using Review manager 5.3 software. RESULTS 22 articles were selected with a total sample size of 178033. The pooled prevalence of H. pylori was 42% (95%CI: 37% to 47%) and mean difference of BMI between subjects with and without H. pylori infection was 0.94 (95%CI: -0.04 to 1.91). 9 eligible studies with 27111 subjects were used to calculated pooled OR value because they contained obesity groups. The OR value showed that H. pylori-positive subjects tended to be obese at a risk of 1.20 (95% CI: 1.13 to 1.28). CONCLUSION In China, obesity has association with H. pylori infection. H. pylori infection may be one of the risk factors for obesity.
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Affiliation(s)
- Xinlan Xu
- School of Mathematics and Statistics, Lanzhou University, Lanzhou, Gansu, China
| | - Weide Li
- School of Mathematics and Statistics, Lanzhou University, Lanzhou, Gansu, China
| | - Lan Qin
- School of Mathematics and Statistics, Lanzhou University, Lanzhou, Gansu, China
| | - Wenjiao Yang
- School of Public Health, Lanzhou University, Lanzhou, Gansu, China
| | - Guowei Yu
- Medical College of Northwest University for Nationalities, Lanzhou, Gansu, China
| | - Qishan Wei
- Maternal and Child Health Hospital, Lanzhou, Gansu, China
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26
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Mansour-Ghanaei F, Joukar F, Baghaee M, Sepehrimanesh M, Hojati A. Only serum pepsinogen I and pepsinogen I/II ratio are specific and sensitive biomarkers for screening of gastric cancer. Biomol Concepts 2019; 10:82-90. [PMID: 31188744 DOI: 10.1515/bmc-2019-0010] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/28/2018] [Accepted: 03/12/2019] [Indexed: 02/06/2023] Open
Abstract
Purpose We aimed to determine optimal cut-off points of plasma levels of ghrelin and serum levels of pepsinogen I, II, and their ratio for screening of gastric cancer (GC). Methods Blood samples were taken from 41 patients with confirmed gastric cancer along with 82 patients without malignancy. Serum levels of pepsinogen I and II, plus plasma levels of acylated ghrelin were measured using commercial ELISA kits. Results The case group had significant lower plasma levels of ghrelin, pepsinogen I, and pepsinogen I/II ratio in comparison to the control group (P<0.001). In the control group, there was significant higher serum pepsinogen I (P=0.028) and pepsinogen II (P=0.003) and lower pepsinogen I/II ratio (P=0.020) in males versus females; significantly higher serum pepsinogen II (P=0.047) and lower pepsinogen I/II ratio (P=0.030) in overweight compared to normal weight patients; and significantly lower pepsinogen I/II ratio (P=0.030) in smokers versus non-smoker. In the case group, there was only significantly lower pepsinogen I (P=0.006) in males versus females, and significantly lower plasma ghrelin (P=0.017) in overweight compared to normal weight patients. The characteristic curve analysis indicated that pepsinogen I at a cut-off of 70.95 μg/L and pepsinogen I/II ratio at cut-off of 2.99, had good sensitivity and specificity. Conclusions Just serums levels of pepsinogen I and the ratio of pepsinogen I/II can be used as biomarker to screen GC.
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Affiliation(s)
- Fariborz Mansour-Ghanaei
- Gastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences, Rasht, Iran
| | - Farahnaz Joukar
- Gastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences, Rasht, Iran
| | - Massood Baghaee
- GI Cancer Screening and Prevention Research Center, Guilan University of Medical Sciences, Guilan University of Medical Sciences, Rasht, Iran
| | - Masood Sepehrimanesh
- GI Cancer Screening and Prevention Research Center, Guilan University of Medical Sciences, Guilan University of Medical Sciences, Rasht, Iran
| | - Amineh Hojati
- Caspian Digestive Diseases Research Center,Guilan University of Medical Sciences, Rasht, Iran
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27
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Hosseininasab Nodoushan SA, Nabavi A. The Interaction of Helicobacter pylori Infection and Type 2 Diabetes Mellitus. Adv Biomed Res 2019; 8:15. [PMID: 30993085 PMCID: PMC6425747 DOI: 10.4103/abr.abr_37_18] [Citation(s) in RCA: 29] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022] Open
Abstract
Helicobacter pylori is one of the most common human pathogens that can cause gastrointestinal (GI) disorders, including simple gastritis, gastric ulcer, and malignant gastritis. In some cases, such as immunodeficiency and underlying diseases, it can be problematic as opportunistic infections. Diabetes mellitus (type 2) (T2DM) is one of the H. pylori underlying diseases. Since GI problems are observed in diabetic patients, it is necessary to treat H. pylori infection. In this review, we aimed to evaluate the possible relationship between H. pylori and T2DM according to epidemiological surveys of 70 studies retrieved from databases, including Scopus, PubMed, and Google Scholar about the relationship between H. pylori and T2DM, and discuss the reported background mechanisms of this correlation. According to the results of our study, the different studies have shown that H. pylori is more prevalent in Type 2 diabetic patients than healthy individuals or nondiabetic patients. The reason is development of H. pylori infection-induced inflammation and production of inflammatory cytokines as well as different hormonal imbalance by this bacterium, which are associated with diabetes mellitus. On the other hand, by tracing anti-H. pylori antibodies in patients with diabetes mellitus and occurrence of symptoms such as digestive problems in >75% of these patients, it can be concluded that there is a relationship between this bacterium and T2DM. Considering the evidence, it is crucially important that the probability of infection with H. pylori is evaluated in patients with T2DM so that medical process of the patient is followed with higher cautious.
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Affiliation(s)
| | - Amin Nabavi
- Department of Biochemistry, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
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28
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Osawa H, Miura Y, Takezawa T, Ino Y, Khurelbaatar T, Sagara Y, Lefor AK, Yamamoto H. Linked Color Imaging and Blue Laser Imaging for Upper Gastrointestinal Screening. Clin Endosc 2018; 51:513-526. [PMID: 30384402 PMCID: PMC6283759 DOI: 10.5946/ce.2018.132] [Citation(s) in RCA: 47] [Impact Index Per Article: 6.7] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/31/2018] [Revised: 09/15/2018] [Accepted: 09/18/2018] [Indexed: 12/16/2022] Open
Abstract
White light imaging (WLI) may not reveal early upper gastrointestinal cancers. Linked color imaging (LCI) produces bright images in the distant view and is performed for the same screening indications as WLI. LCI and blue laser imaging (BLI) provide excellent visibility of gastric cancers in high color contrast with respect to the surrounding tissue. The characteristic purple and green color of metaplasias on LCI and BLI, respectively, serve to increase the contrast while visualizing gastric cancers regardless of a history of Helicobacter pylori eradication. LCI facilitates color-based recognition of early gastric cancers of all morphological types, including flat lesions or those in an H. pylori-negative normal background mucosa as well as the diagnosis of inflamed mucosae including erosions. LCI reveals changes in mucosal color before the appearance of morphological changes in various gastric lesions. BLI is superior to LCI in the detection of early esophageal cancers and abnormal findings of microstructure and microvasculature in close-up views of upper gastrointestinal cancers. Excellent images can also be obtained with transnasal endoscopy. Using a combination of these modalities allows one to obtain images useful for establishing a diagnosis. It is important to observe esophageal cancers (brown) using BLI and gastric cancers (orange) surrounded by intestinal metaplasia (purple) and duodenal cancers (orange) by LCI.
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Affiliation(s)
- Hiroyuki Osawa
- Division of Gastroenterology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan
| | - Yoshimasa Miura
- Division of Gastroenterology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan
| | - Takahito Takezawa
- Division of Gastroenterology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan
| | - Yuji Ino
- Division of Gastroenterology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan
| | - Tsevelnorov Khurelbaatar
- Division of Gastroenterology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan
| | - Yuichi Sagara
- Division of Gastroenterology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan
| | - Alan Kawarai Lefor
- Department of Medicine, Department of Surgery, Jichi Medical University, Shimotsuke, Japan
| | - Hironori Yamamoto
- Division of Gastroenterology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan
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29
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Adachi K, Mishiro T, Okimoto E, Kinoshita Y. Influence of the Degree of Gastric Mucosal Atrophy on the Serum Lipid Levels Before and After the Eradication of Helicobacter pylori Infection. Intern Med 2018; 57:3067-3073. [PMID: 29877271 PMCID: PMC6262702 DOI: 10.2169/internalmedicine.1074-18] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/20/2022] Open
Abstract
Objective To clarify the influence of the degree of gastric mucosal atrophy on the serum lipid levels before and after the eradication of Helicobacter pylori infection. Methods The subjects were individuals who underwent an annual detailed medical checkup. Serum anti-H. pylori IgG antibody detection and upper endoscopic examinations were performed in all subjects. Gastric mucosal atrophy was evaluated by the classification of Kimura and Takemoto. The serum levels of total cholesterol, high-density lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), LDLC/HDLC ratio, and triglycerides were compared among the different degrees of gastric mucosal atrophy in H. pylori-positive subjects. In addition, changes in those serum lipid levels during a two-year period were compared among H. pylori post-eradication cases that showed different degrees of gastric mucosal atrophy prior to eradication. Results In subjects with higher degrees of gastric mucosal atrophy, the serum levels of total cholesterol, LDLC, and triglycerides were elevated. Furthermore, the LDLC/HDLC ratio in subjects with moderate and severe grades of gastric mucosal atrophy was significantly higher than in subjects with mild atrophy. In subjects with higher degrees of gastric mucosal atrophy, the serum level of LDLC and the LDLC/HDLC ratio were decreased following eradication of H. pylori. Conclusion Lipid metabolism is influenced by the degree of gastric mucosal atrophy present before the eradication of H. pylori, and the favorable effects of such eradication are significant in patients with higher degrees of atrophy.
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Affiliation(s)
- Kyoichi Adachi
- Health Center, Shimane Environment and Health Public Corporation, Japan
| | - Tomoko Mishiro
- Health Center, Shimane Environment and Health Public Corporation, Japan
| | - Eiko Okimoto
- Health Center, Shimane Environment and Health Public Corporation, Japan
| | - Yoshikazu Kinoshita
- Second Department of Internal Medicine, Shimane University Faculty of Medicine, Japan
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Oral hydroxysafflor yellow A reduces obesity in mice by modulating the gut microbiota and serum metabolism. Pharmacol Res 2018; 134:40-50. [PMID: 29787870 DOI: 10.1016/j.phrs.2018.05.012] [Citation(s) in RCA: 151] [Impact Index Per Article: 21.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/10/2018] [Revised: 04/25/2018] [Accepted: 05/17/2018] [Indexed: 12/18/2022]
Abstract
Given the high and increasing prevalence of obesity, the safe and effective treatment of obesity would be beneficial. Here, we examined whether oral hydroxysafflor yellow A (HSYA), an active compound from the dried florets of Carthamus tinctorius L., can reduce high-fat (HF) diet-induced obesity in C57BL/6 J mice. Our results showed that the average body weight of HF group treated by HSYA was significantly lower than that of the HF group (P < 0.01). HSYA also reduced fat accumulation, ameliorated insulin resistance, restored glucose homeostasis, reduced inflammation, enhanced intestinal integrity, and increased short-chain fatty acids (SCFAs) production in HF diet-fed mice. Sequencing of 16S rRNA genes in fecal samples demonstrated that HSYA reversed HF diet induced gut microbiota dysbiosis. Particularly, HSYA increased the relative abundances of genera Akkermansia and Romboutsia, as well as SCFAs-producing bacteria, including genera Butyricimonas and Alloprevotella, whereas it decreased the phyla Firmicutes/Bacteroidetes ratio of HF diet-fed mice. Additionally, serum metabolomics analysis revealed that HSYA increased lysophosphatidylcholines (lysoPCs), L-carnitine and sphingomyelin, and decreased phosphatidylcholines in mice fed a HF diet, as compared to HF group. These changed metabolites were mainly linked with the pathways of glycerophospholipid metabolism and sphingolipid metabolism. Spearman's correlation analysis further revealed that Firmicutes was positively while Bacteroidetes and Akkermansia were negatively correlated with body weight, fasting serum glucose and insulin. Moreover, Akkermansia and Butyricimonas had positive correlations with lysoPCs, suggestive of the role of gut microbiota in serum metabolites. Our findings suggest HSYA may be a potential therapeutic drug for obesity and the gut microbiota may be potential territory for targeting of HSYA.
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Sugimoto M, Yasuda H, Andoh A. Nutrition status and Helicobacter pylori infection in patients receiving hemodialysis. World J Gastroenterol 2018; 24:1591-1600. [PMID: 29686466 PMCID: PMC5910542 DOI: 10.3748/wjg.v24.i15.1591] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/23/2018] [Revised: 03/18/2018] [Accepted: 03/25/2018] [Indexed: 02/06/2023] Open
Abstract
Chronic kidney disease (CKD) patients receiving hemodialysis (HD) often develop gastrointestinal abnormalities over their long treatment period. In general, prognosis in such patients is poor due to the development of protein-energy wasting (PEW). Therefore, it is important to clarify the etiology of PEW and to establish better strategies to deal with this condition. Chronic Helicobacter pylori (H. pylori) infection in the gastric mucosa has a close association with not only the development of peptic ulcer disease and gastric cancer, but is also associated with abnormal plasma and gastric mucosal ghrelin levels that are seen in malnutrition. It is unclear whether H. pylori infection of the gastric mucosa is directly associated with prognosis in HD patients by affecting ghrelin levels. Recent studies show that the prevalence of H. pylori infection in HD patients is significantly lower than in subjects with normal renal function. In the natural history of H. pylori infection in HD patients, the prevalence of infection decreases as the length of time on HD increases. The severity of gastric mucosal atrophy has been suggested as the major determinant of ghrelin levels in these patients, and eradication therapy of H. pylori improves nutritional status by increasing serum cholinesterase and cholesterol levels, especially in patients with mild-to-moderate gastric mucosal atrophy. Prompt H. pylori eradication to inhibit the progress of gastric atrophy may be required to prevent this decrease in ghrelin levels and subsequent PEW and improve the prognosis of HD patients by improving their nutritional status.
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Affiliation(s)
- Mitsushige Sugimoto
- Division of Digestive Endoscopy, Shiga University of Medical Science Hospital, Shiga 520-2192, Japan
| | - Hideo Yasuda
- First Department of Medicine, Hamamatsu University School of Medicine, Shizuoka 431-3192, Japan
| | - Akira Andoh
- Department of Gastroenterology, Shiga University of Medical Science Hospital, Shiga 520-2192, Japan
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Possible association of ghrelin/obestatin balance with cardiometabolic risk in obese subjects with Helicobacter pylori. Endocr Regul 2018; 52:101-109. [PMID: 29715187 DOI: 10.2478/enr-2018-0012] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/18/2022] Open
Abstract
OBJECTIVES Helicobacter pylori (H. pylori) is a common gastric infection associated with extragastric conditions. The association between H. pylori infection and obesity is unclear. H. pylori may affect gut hormones involved in food intake and energy expenditure. The aim of this study is to evaluate ghrelin/obestatin balance and leptin in obese subjects with H. pylori infection. METHODS Sixty healthy volunteers were divided into: obese and non-obese groups. Each group was divided into H. Pylori positive or H. pylori negative. Anthropometric parameters, H. pylori status, serum glucose, insulin level, and lipid profile were estimated with calculation of Homeostasis Model Assessment Insulin Resistance (HOMA-IR). Serum levels of ghrelin, obestatin, and leptin were evaluated. RESULTS Significant increase was found in serum glucose, insulin and HOMA-IR ratio in obese subjects with positive H. pylori as compared to other groups. H. pylori positive obese subjects showed significantly increased ghrelin, ghrelin/obestatin balance, and leptin with a significant decrease in obestatin as compared to negative subjects. Ghrelin/obestatin ratio positively correlated with weight, body mass index, waist, glucose, insulin, HOMA-IR, leptin, cholesterol, triglycerides, low density cholesterol and also with H. pylori antigen in the same group. CONCLUSIONS It can be concluded that ghrelin, obestatin, and leptin are affected by presence of H. pylori seropositivity in obese subjects. The higher ghrelin levels and ghrelin/obestatin ratio with lowered obestatin could be considered as a gastro-protective effect against inflammation induced by H. pylori.
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Adachi K, Mishiro T, Toda T, Kano N, Fujihara H, Mishima Y, Konishi A, Mochida M, Takahashi K, Kinoshita Y. Effects of Helicobacter pylori eradication on serum lipid levels. J Clin Biochem Nutr 2018; 62:264-269. [PMID: 29892167 PMCID: PMC5990401 DOI: 10.3164/jcbn.17-88] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/05/2017] [Accepted: 11/05/2017] [Indexed: 12/17/2022] Open
Abstract
The purpose was to clarify the effects of Helicobacter pylori (H. pylori) eradication on the changes in serum lipid levels by comparing subjects with and without continuous H. pylori infection. The study subjects were 774 individuals (males 536, females 238, mean age 52.6 years) who visited between April 2013 and March 2016 for annual medical checkups. Serum total cholesterol, high-density lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), and triglyceride levels, and LDLC/HDLC ratio were compared between the subjects with and without H. pylori infection, as well as those with H. pylori eradication subjects. The HDLC level in the H. pylori-positive group was significantly lower as compared to the H. pylori-negative group. The serum level of HDLC in subjects with successful eradication of H. pylori tended to be higher, while the serum levels of total cholesterol, LDLC, and triglycerides tended to be lower in comparison to subjects with continuous H. pylori infection. In addition, the LDLC/HDLC ratio in the H. pylori-positive group was significantly higher than that in the H. pylori-negative group, and successful H. pylori eradication tended to reduce that ratio. In conclusion, successful eradication of H. pylori may have favorable effects on lipid metabolism.
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Affiliation(s)
- Kyoichi Adachi
- Health Center, Shimane Environment and Health Public Corporation, Koshibara 1-4-6, Matsue, Shimane 690-0012, Japan
| | - Tomoko Mishiro
- Health Center, Shimane Environment and Health Public Corporation, Koshibara 1-4-6, Matsue, Shimane 690-0012, Japan
| | - Takashi Toda
- Clinical Laboratory, Shimane Environment and Health Public Corporation, Matsue, Shimane 690-0012, Japan
| | - Naomi Kano
- Clinical Laboratory, Shimane Environment and Health Public Corporation, Matsue, Shimane 690-0012, Japan
| | - Harumi Fujihara
- Clinical Laboratory, Shimane Environment and Health Public Corporation, Matsue, Shimane 690-0012, Japan
| | - Yuko Mishima
- Clinical Laboratory, Shimane Environment and Health Public Corporation, Matsue, Shimane 690-0012, Japan
| | - Atsuko Konishi
- Clinical Laboratory, Shimane Environment and Health Public Corporation, Matsue, Shimane 690-0012, Japan
| | - Mariko Mochida
- Health Center, Shimane Environment and Health Public Corporation, Koshibara 1-4-6, Matsue, Shimane 690-0012, Japan
| | - Kazuko Takahashi
- Health Center, Shimane Environment and Health Public Corporation, Koshibara 1-4-6, Matsue, Shimane 690-0012, Japan
| | - Yoshikazu Kinoshita
- Second Department of Internal Medicine, Shimane University Faculty of Medicine, Izumo, Shimane 693-8501, Japan
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Yanagi H, Tsuda A, Matsushima M, Takahashi S, Ozawa G, Koga Y, Takagi A. Changes in the gut microbiota composition and the plasma ghrelin level in patients with Helicobacter pylori-infected patients with eradication therapy. BMJ Open Gastroenterol 2017; 4:e000182. [PMID: 29225907 PMCID: PMC5717420 DOI: 10.1136/bmjgast-2017-000182] [Citation(s) in RCA: 44] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/09/2017] [Accepted: 11/08/2017] [Indexed: 12/20/2022] Open
Abstract
Objective To investigate the influence of antimicrobials on both the gut microbiota structure and the plasma ghrelin level using Helicobacter pylori-infected patients who underwent eradication therapy. Design Twenty H. pylori-infected patients (mean age 68.3 years old) who underwent eradication therapy participated in the study. For the therapy, patients had 1 week of triple therapy consisting of amoxicillin, clarithromycin and proton-pump inhibitors. Stool and blood samples were obtained before (S1), immediately after (S2) and/or 3 months after (S3) the therapies. The concentrations of ghrelin and leptin in the blood were assayed using an ELISA. The V3-V4 region of the 16S rRNA gene was amplified using bacterial DNA from the stool, and about 50 000 high-quality amplicons per sample were grouped into operational taxonomic units for bacteriological analyses. Results The Bacteroidetes:Firmicutes (B:F) ratio was significantly greater at S3 than S1 (P<0.01). This increase in the B:F ratio between S3 and S1 was found in 15 out of 20 patients. A significant decrease in the concentration of active ghrelin (P=0.003) in the plasma was observed between S3 and S1. There was a statistically significant correlation between the rate of patients whose B:F ratio increased and that of patients whose active ghrelin level decreased between S3 and S1 according to Fisher’s exact probability test (P=0.03). Conclusions Changes in the gut microbiota, such as the B:F ratio after treatment with antimicrobials, might cause a change in the plasma ghrelin level, as the direct and earliest target of antimicrobials would be the microbiota rather than the hormone-secreting system.
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Affiliation(s)
- Hidetaka Yanagi
- Department of General Medicine, Tokai University School of Medicine, Isehara, Japan
| | - Ayumi Tsuda
- Department of General Medicine, Tokai University School of Medicine, Isehara, Japan
| | - Masashi Matsushima
- Department of Gastroenterology, Tokai University School of Medicine, Isehara, Japan
| | | | - Genki Ozawa
- Technical Department, TechnoSuruga Laboratory Co. Ltd, Shizuoka, Japan
| | - Yasuhiro Koga
- Laboratory for Infectious Diseases, Tokai University School of Medicine, Isehata, Japan
| | - Atsushi Takagi
- Department of General Medicine, Tokai University School of Medicine, Isehara, Japan
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Kountouras J, Polyzos SA, Katsinelos P, Doulberis M, Zavos C, Kazakos E, Boziki M, Tzivras D, Kotronis G. Letter: Helicobacter pylori in lean and obese patients with non-alcoholic fatty liver disease. Aliment Pharmacol Ther 2017; 46:637-638. [PMID: 28805327 DOI: 10.1111/apt.14222] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Affiliation(s)
- J Kountouras
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - S A Polyzos
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - P Katsinelos
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - M Doulberis
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - C Zavos
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - E Kazakos
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - M Boziki
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - D Tzivras
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
| | - G Kotronis
- Department of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Greece
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Association Between Helicobacter Pylori Infection and Insulin Resistance: A Systematic Review. ROMANIAN JOURNAL OF DIABETES NUTRITION AND METABOLIC DISEASES 2017. [DOI: 10.1515/rjdnmd-2017-0019] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/22/2023] Open
Abstract
Abstract
Most studies in the past decades show that screening of Helicobacter Pylori (HP) together with monitoring the inflammatory markers, plasma glucose and HbA1c levels can help prevent or delay type 2 diabetes mellitus. There is a double interrelation between HP infection and diabetes; thus diabetic patients are more susceptible to infection with HP via multiple mechanisms (decreased cellular and humoral immunity induced by diabetes, reducing gastrointestinal motility and secretion of hydrochloric acid, impaired glucose metabolism with the advent of chemical modifications of the gastric mucosa, the last two mechanisms favoring the intestinal colonization with HP). At the same time, those infected with HP can develop diabetes. The purpose of this paper is reviewing the data from the medical literature on the role of the chronic infection with HP on the induction of type 2 diabetes. The studies presented below lead us to the conclusion that the chronic infection with HP, in addition to local specific effects (simple gastritis, peptic ulcer and malignant diseases), also has extradigestive effects. The one approached in our work is that HP is being able to induce type 2 diabetes by complex mechanisms related to insulin resistance, chronic low-grade inflammation, decreased insulin secretion, and influences on glucose and lipid absorption.
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Slomiany BL, Slomiany A. Role of LPS-elicited signaling in triggering gastric mucosal inflammatory responses to H. pylori: modulatory effect of ghrelin. Inflammopharmacology 2017; 25:415-429. [PMID: 28516374 DOI: 10.1007/s10787-017-0360-1] [Citation(s) in RCA: 26] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/07/2017] [Accepted: 05/05/2017] [Indexed: 12/14/2022]
Abstract
Infection with Helicobacter pylori is a primary culprit in the etiology of gastric disease, and its cell-wall lipopolysaccharide (LPS) is recognized as a potent endotoxin responsible for triggering a pattern of the mucosal inflammatory responses. The engagement by the LPS of gastric mucosal Toll-like receptor 4 (TLR4) leads to initiation of signal transduction events characterized by the activation of mitogen-activated protein kinase (MAPK) cascade, induction of phosphoinositide-specific phospholipase C (PLC)/protein kinase C (PKC)/phosphatidylinositol 3-kinase (PI3K) pathway, and up-regulation in Src/Akt. These signaling events in turn exert their influence over H. pylori-elicited excessive generation of NO and PGE2 caused by the disturbances in nitric oxide synthase and cyclooxygenase isozyme systems, increase in epidermal growth factor receptor transactivation, and the induction in matrix metalloproteinase-9 (MMP-9) release. Interestingly, the extent of gastric mucosal inflammatory response to H. pylori is influenced by a peptide hormone, ghrelin, the action of which relays on the growth hormone secretagogue receptor type 1a (GHS-R1a)-mediated mobilization of G-protein dependent transduction pathways. Yet, the signals triggered by TLR-4 activation as well as those arising through GHS-R1a stimulation converge at MAPK and PLC/PKC/PI3K pathways that form a key integration node for proinflammatory signals generated by H. pylori LPS as well as for those involved in modulation of inflammation by ghrelin. Hence, therapeutic targeting these signals' convergence and integration node could provide a novel and attractive opportunities for developing more effective treatments of H. pylori-related gastric disease.
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Affiliation(s)
- B L Slomiany
- Research Center, C855, Rutgers School of Dental Medicine, Rutgers, The State University of New Jersey, 110 Bergen Street, PO Box 1709, Newark, NJ, 07103-2400, USA
| | - A Slomiany
- Research Center, C855, Rutgers School of Dental Medicine, Rutgers, The State University of New Jersey, 110 Bergen Street, PO Box 1709, Newark, NJ, 07103-2400, USA.
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Xu MY, Liu L, Yuan BS, Yin J, Lu QB. Association of obesity with Helicobacter pylori infection: A retrospective study. World J Gastroenterol 2017; 23:2750-2756. [PMID: 28487612 PMCID: PMC5403754 DOI: 10.3748/wjg.v23.i15.2750] [Citation(s) in RCA: 32] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/12/2016] [Revised: 01/17/2017] [Accepted: 03/15/2017] [Indexed: 02/06/2023] Open
Abstract
AIM To explore the association between Helicobacter pylori (H. pylori) infection and obesity/weight gain in a Chinese population.
METHODS Our primary outcome was the change in body mass index (BMI). The generalized linear models were used to explore the association between H. pylori infection and the change of BMI, and the logistic regression models were used to explore the association between H. pylori infection and obesity.
RESULTS A total of 3039 subjects were recruited and analyzed, of which 12.8% were obese. The prevalence of H. pylori infection was 53.9% (1639/3039) overall and 54.6% (212/388) in the obese subjects. The change of BMI in the H. pylori (+) group was not significantly higher than that in the H. pylori (-) group after adjustment for potential confounding factors [RR = 0.988, 95%CI: 0.924-1.057, P = 0.729]. The prevalence of obesity decreased 1.1% in the H. pylori (+) group and 0.5% in the H. pylori (-) group. The RR of H. pylori infection for obesity was 0.831 (95%CI: 0.577-1.197, P = 0.321) after the adjustment.
CONCLUSION H. pylori infection was not associated with overweight/obesity observed from the retrospective study in this Chinese population.
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Kim SH, Kim JW, Byun J, Jeong JB, Kim BG, Lee KL. Plasma ghrelin level and plasma ghrelin/obestatin ratio are related to intestinal metaplasia in elderly patients with functional dyspepsia. PLoS One 2017; 12:e0175231. [PMID: 28419119 PMCID: PMC5395142 DOI: 10.1371/journal.pone.0175231] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/30/2016] [Accepted: 03/22/2017] [Indexed: 12/19/2022] Open
Abstract
Background Whether plasma ghrelin/obestatin levels are associated with Helicobacter pylori (H. pylori) infection, subtypes of functional dyspepsia (FD), and gastric mucosal histology has not yet been established in elderly patients. Objective The aim of this study was to determine whether plasma ghrelin and obestatin levels are related to gastric mucosal histology, H. pylori infection, and FD subtypes in elderly patients with FD. Methods Ninety-two patients diagnosed with FD and older than 60 years (median age 69.4; range 60–88) were included. Clinical symptoms investigated included postprandial fullness, epigastric pain, epigastric soreness, nausea, and vomiting. According to the Rome III criteria, patients diagnosed with FD were divided into two subtypes: epigastric pain syndrome (EPS) and postprandial distress syndrome (PDS). Plasma ghrelin and obestatin levels were measured using enzyme immunoassay, and histological examination of gastric mucosa was performed. H. pylori infection was determined by histopathological examination of gastric mucosal biopsy and/or Campylobacter-like organism test. Results In our study, plasma ghrelin levels and plasma ghrelin/obestatin (G/O) ratio were significantly lower in subjects with intestinal metaplasia compared with those without intestinal metaplasia (ghrelin, p = 0.010; G/O ratio, p = 0.012). On the other hand, there were no significant differences in plasma ghrelin and obestatin levels between H. pylori–positive and H. pylori–negative groups. (ghrelin, p = 0.130; obestatin, p = 0.888). Similarly, no significant differences were detected between the EPS and PDS groups (ghrelin, p = 0.238; obestatin, p = 0.710). Conclusions Patients with intestinal metaplasia, a known precursor of gastric cancer, had significantly less plasma ghrelin levels and G/O ratio than those without intestinal metaplasia.
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Affiliation(s)
- Su Hwan Kim
- Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul, Republic of Korea
| | - Ji Won Kim
- Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul, Republic of Korea
- * E-mail:
| | - Junsu Byun
- Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul, Republic of Korea
| | - Ji Bong Jeong
- Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul, Republic of Korea
| | - Byeong Gwan Kim
- Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul, Republic of Korea
| | - Kook Lae Lee
- Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul, Republic of Korea
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Ichikawa H, Sugimoto M, Sakao Y, Sahara S, Ohashi N, Kato A, Sugimoto K, Furuta T, Andoh A, Sakao T, Yasuda H. Relationship between ghrelin, Helicobacter pylori and gastric mucosal atrophy in hemodialysis patients. World J Gastroenterol 2016; 22:10440-10449. [PMID: 28058025 PMCID: PMC5175257 DOI: 10.3748/wjg.v22.i47.10440] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/27/2016] [Revised: 10/18/2016] [Accepted: 11/13/2016] [Indexed: 02/06/2023] Open
Abstract
AIM To investigate the relationship between plasma ghrelin level, Helicobacter pylori (H. pylori) infection status and the severity of atrophy in hemodialysis patients.
METHODS One hundred eights patients who received hemodialysis and 13 non-hemodialysis H. pylori-negative controls underwent gastroduodenoscopy to evaluate the severity of gastric atrophy. Serum levels of pepsinogen (PG) were measured as serum markers of gastric atrophy. H. pylori infection was evaluated by anti-H. pylori IgG antibody, rapid urease test and culture test. We classified H. pylori infection status as non-infection, present infection and past infection. In addition, plasma acyl-ghrelin and desacyl-ghrelin levels were measured by enzyme-linked immunosorbent assay.
RESULTS Infection rate of H. pylori was 45.4% (49/108). Acyl-ghrelin level in the non-infection group (39.4 ± 23.0 fmol/mL) was significantly higher than in the past (23.4 ± 19.9 fmol/mL, P = 0.005) and present infection groups (19.5 ± 14.0 fmol/mL, P < 0.001). Furthermore, desacyl-ghrelin level in the non-infection group (353.2 ± 190.2 fmol/mL) was significantly higher than those in the past (234.9 ± 137.5 fmol/mL, P = 0.008) and present infection groups (211.8 ± 124.2 fmol/mL, P < 0.001). Acyl-ghrelin was positively correlated with the PG I level and PG I/II ratio (|R| = 0.484, P < 0.001 and |R| = 0.403, P < 0.001, respectively). Both ghrelins were significantly decreased in accordance with the progress of endoscopic atrophy (both P < 0.001) and acyl-ghrelin was significantly lower in patients with mild, moderate and severe atrophy (24.5 ± 23.1 fmol/mL, 20.2 ± 14.9 fmol/mL and 18.3 ± 11.8 fmol/mL) than in those with non-atrophy (39.4 ± 22.2 fmol/mL, P = 0.039, P = 0.002 and P < 0.001, respectively).
CONCLUSION In hemodialysis patients, plasma ghrelin level was associated with the endoscopic and serological severity of atrophy related to H. pylori infection.
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Lecube A, Valladares S, López-Cano C, Gutiérrez L, Ciudin A, Fort JM, Reñé JM, Matias-Guiu X, de Torres I, Bueno M, Pallarés J, Baena JA. The Role of Morbid Obesity in the Promotion of Metabolic Disruptions and Non-Alcoholic Steatohepatitis by Helicobacter Pylori. PLoS One 2016; 11:e0166741. [PMID: 27893763 PMCID: PMC5125598 DOI: 10.1371/journal.pone.0166741] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/15/2016] [Accepted: 11/02/2016] [Indexed: 12/13/2022] Open
Abstract
Background Helicobacter pylory (HP) infection has been associated to an increased rate of type 2 diabetes (T2D) and liver disease through its effect on insulin resistance and systemic inflammation. However, results are inconstant and no studies exist in morbidly obese patients, in which both insulin resistance and inflammation coexist. Material and Methods Cross-sectional study to evaluate the relationship between HP infection and alterations in carbohydrate metabolism, lipid profile, inflammation markers, and liver disease in patients awaiting for bariatric surgery. HP infection was histologically assessed in gastric antrum biopsy from 416 subjects. Liver biopsy was also available in 93 subjects. Results Both impaired fasting glucose and T2D were similar when comparing subjects with and without HP infection (24.2% vs. 22%, p = 0.290 and 29.4% vs. 29.1%, p = 0.916, respectively), with no differences between groups in the HOMA-IR, lipid profile neither inflammatory parameters. However, HP infection was higher among subjects with a BMI ≥ 40.0 kg/m2 in comparison with lower degrees of obesity (71.7% vs. 60.0%, p = 0.041). In addition, subjects without HP infection showed higher degrees of steatosis (44.1±26.4% vs. 32.0±20.7%, p = 0.038), as well as a lower prevalence of non-alcoholic steatohepatitis (9.3% vs. 30.7%, p = 0.023). Conclusions In patients with morbid obesity, HP infection does not seem to be associated with abnormal carbohydrate metabolism. In addition, less advanced degrees of non-alcoholic fatty disease were observed. We suggest that low-grade inflammation that accompanies obesity mitigates the diabetogenic effect of HP, so the presence of obesity should be considered in studies that evaluate the HP metabolic effects.
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Affiliation(s)
- Albert Lecube
- Endocrinology and Nutrition Department, EASO Collaborating Centre for Obesity Management, Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
- CIBER de Diabetes y Enfermedades Metabólicas asociadas (CIBEREM), Instituto de Salud Carlos III (ISCIII), Madrid, Spain
- * E-mail:
| | - Silvia Valladares
- Endocrinology and Nutrition Department, EASO Collaborating Centre for Obesity Management, Vall d’Hebron University Hospital, Vall d’Hebron Institut de Recerca (VHIR), Autonomous University of Barcelona, Barcelona, Spain
| | - Carolina López-Cano
- Endocrinology and Nutrition Department, EASO Collaborating Centre for Obesity Management, Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
| | - Liliana Gutiérrez
- Endocrinology and Nutrition Department, EASO Collaborating Centre for Obesity Management, Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
| | - Andreea Ciudin
- Endocrinology and Nutrition Department, EASO Collaborating Centre for Obesity Management, Vall d’Hebron University Hospital, Vall d’Hebron Institut de Recerca (VHIR), Autonomous University of Barcelona, Barcelona, Spain
| | - José Manuel Fort
- Endocrine, Bariatric and Metabolic Surgery Unit, IFSO Centre of Excellence, Vall d’Hebron University Hospital, Vall d’Hebron Institut de Recerca (VHIR), Autonomous University of Barcelona, Barcelona, Spain
| | - Josep Maria Reñé
- Gastroenterology Department. Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
| | - Xavier Matias-Guiu
- Department of Pathology and Molecular Genetics, Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
| | - Inés de Torres
- Pathology Department, Vall d’Hebron University Hospital, Vall d’Hebron Institut de Recerca (VHIR), Autonomous University of Barcelona, Barcelona, Spain
| | - Marta Bueno
- Endocrinology and Nutrition Department, EASO Collaborating Centre for Obesity Management, Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
| | - Judit Pallarés
- Department of Pathology and Molecular Genetics, Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
| | - Juan Antonio Baena
- Gastrointestinal Surgery Department. Arnau de Vilanova University Hospital, Institut de Recerca Biomèdica (IRB) and University of Lleida, Lleida, Spain
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Kasai C, Sugimoto K, Moritani I, Tanaka J, Oya Y, Inoue H, Tameda M, Shiraki K, Ito M, Takei Y, Takase K. Changes in plasma ghrelin and leptin levels in patients with peptic ulcer and gastritis following eradication of Helicobacter pylori infection. BMC Gastroenterol 2016; 16:119. [PMID: 27716077 PMCID: PMC5050848 DOI: 10.1186/s12876-016-0532-2] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/05/2016] [Accepted: 09/17/2016] [Indexed: 12/17/2022] Open
Abstract
Background Helicobacter pylori (H. pylori) infection and eradication therapy have been known to influence gastric ghrelin and leptin secretion, which may lead to weight gain. However, the exact relationship between plasma ghrelin/leptin levels and H. pylori infection has remained controversial. The aim of this study was to investigate plasma ghrelin and leptin levels in H. pylori-positive and -negative patients, to compare the two levels of the hormones before and after H. pylori eradication, and to examine the correlation between body mass index (BMI) and active ghrelin or leptin levels, as well as that between atrophic pattern and active ghrelin or leptin levels. Methods Seventy-two H. pylori-positive patients who underwent upper gastrointestinal endoscopy, 46 diagnosed as having peptic ulcer and 26 as atrophic gastritis, were enrolled. Control samples were obtained from 15 healthy H. pylori-negative volunteers. The extent of atrophic change of the gastric mucosa was assessed endoscopically. Body weight was measured and blood was collected before and 12 weeks after H. pylori eradication therapy. Blood samples were taken between 8 and 10 AM after an overnight fast. Results Plasma ghrelin levels were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. In particular, plasma active ghrelin levels were significantly lower in patients with gastritis compared with patients with peptic ulcer. Plasma ghrelin levels decreased after H. pylori eradication in both peptic ulcer and gastritis patients, while plasma leptin levels increased only in peptic ulcer patients. Plasma leptin levels and BMI were positively correlated, and active ghrelin levels and atrophic pattern were weakly negatively correlated in peptic ulcer patients. Conclusion H. pylori infection and eradication therapy may affect circulating ghrelin/leptin levels. This finding suggests a relationship between gastric mucosal injury induced by H. pylori infection and changes in plasma ghrelin and leptin levels.
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Affiliation(s)
- Chika Kasai
- Department of Gastroenterology, Mie Prefectural General Medical Center, Yokkaichi, Japan
| | - Kazushi Sugimoto
- Department of Molecular and Laboratory Medicine, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan. .,Department of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu, Japan.
| | - Isao Moritani
- Department of Gastroenterology, Mie Prefectural General Medical Center, Yokkaichi, Japan
| | - Junichiro Tanaka
- Department of Gastroenterology, Mie Prefectural General Medical Center, Yokkaichi, Japan
| | - Yumi Oya
- Department of Gastroenterology, Mie Prefectural General Medical Center, Yokkaichi, Japan
| | - Hidekazu Inoue
- Department of Gastroenterology, Mie Prefectural General Medical Center, Yokkaichi, Japan
| | - Masahiko Tameda
- Department of Molecular and Laboratory Medicine, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan.,Department of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu, Japan
| | - Katsuya Shiraki
- Department of Gastroenterology, Mie Prefectural General Medical Center, Yokkaichi, Japan
| | - Masaaki Ito
- Department of Cardiology and Nephrology, Mie University School of Medicine, Tsu, Japan
| | - Yoshiyuki Takei
- Department of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu, Japan
| | - Kojiro Takase
- Department of Gastroenterology, Mie Prefectural General Medical Center, Yokkaichi, Japan
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He C, Yang Z, Lu N. Imbalance of Gastrointestinal Microbiota in the Pathogenesis of Helicobacter pylori-Associated Diseases. Helicobacter 2016; 21:337-48. [PMID: 26876927 DOI: 10.1111/hel.12297] [Citation(s) in RCA: 35] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
The development of new nucleotide sequencing techniques and advanced bioinformatics tools has opened the field for studying the diversity and complexity of the gastrointestinal microbiome independent of traditional cultural methods. Owing largely to the gastric acid barrier, the human stomach was long thought to be sterile. The discovery of Helicobacter pylori, the gram-negative bacterium that infects upwards of 50% of the global population, has started a major paradigm shift in our understanding of the stomach as an ecologic niche for bacteria. Recent sequencing analysis of gastric microbiota showed that H. pylori was not alone and the interaction of H. pylori with those microorganisms might play a part in H. pylori-associated diseases such as gastric cancer. In this review, we summarize the available literature about the changes of gastrointestinal microbiota after H. pylori infection in humans and animal models, and discuss the possible underlying mechanisms including the alterations of the gastric environment, the secretion of hormones and the degree of inflammatory response. In general, information regarding the composition and function of gastrointestinal microbiome is still in its infancy, future studies are needed to elucidate whether and to what extent H. pylori infection perturbs the established microbiota. It is assumed that clarifying the role of gastrointestinal communities in H. pylori-associated diseases will provide an opportunity for translational application as a biomarker for the risk of serious H. pylori diseases and perhaps identify specific organisms for therapeutic eradication.
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Affiliation(s)
- Cong He
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China
| | - Zhen Yang
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China
| | - Nonghua Lu
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, China.
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Eun Bae S, Hoon Lee J, Soo Park Y, Ok Kim S, Young Choi J, Yong Ahn J, Hoon Kim D, Don Choi K, June Song H, Hyug Lee G, Choe J, Jin Jang S, Jung HY. Decrease of serum total ghrelin in extensive atrophic gastritis: comparison with pepsinogens in histological reference. Scand J Gastroenterol 2016; 51:137-44. [PMID: 26513345 DOI: 10.3109/00365521.2015.1083049] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
OBJECTIVE Ghrelin is mainly secreted by the gastric oxyntic mucosa and its production is impaired in chronic atrophic gastritis. This study aimed at evaluating how serum total ghrelin correlates with the extent of atrophy, and to compare its performance as a serologic marker with that of pepsinogen (PG). MATERIAL AND METHODS Data were collected from 154 patients with atrophic gastritis. The histological extent of atrophy was assessed by three paired biopsies from the antrum, corpus lesser curvature (CLC), and corpus greater curvature (CGC). Fasting serum concentrations of total ghrelin, pepsinogen I and II were measured. Regression analysis was performed to evaluate the factors associated with serum total ghrelin. The serologic performance was compared with that of pepsinogen using receiver-operating characteristic (ROC) curves. RESULTS The Helicobacter pylori infection rate was 85%, and extensive atrophic gastritis involving CGC was found in 24%. Serum total ghrelin was significantly decreased in patients with extensive CGC atrophy (median: 170.4 pg/mL, vs 201.1 pg/mL in patients without atrophy; p < 0.001), and its levels correlated with those of pepsinogen I and I/II ratio. The decrease of serum total ghrelin was independent of age, gender, body mass index (BMI), and H. pylori infection status. The sensitivity and specificity of serum total ghrelin in predicting extensive atrophy were 57% and 79%, respectively. The discriminatory ability was similar to that of pepsinogen I/II ratio (p = 0.612), and lower than that of pepsinogen I (p = 0.040). CONCLUSIONS Serum total ghrelin is decreased during extensive atrophy involving CGC. The serologic performance is lower than that of pepsinogen I.
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Affiliation(s)
- Suh Eun Bae
- a Health Screening and Promotion Center , University of Ulsan College of Medicine, Asan Medical Center , Seoul , South Korea
| | | | | | - Seon Ok Kim
- d Department of Clinical Epidemiology and Biostatistics , University of Ulsan College of Medicine, Asan Medical Center , Seoul , South Korea
| | - Ji Young Choi
- a Health Screening and Promotion Center , University of Ulsan College of Medicine, Asan Medical Center , Seoul , South Korea
| | | | | | | | | | | | - Jaewon Choe
- a Health Screening and Promotion Center , University of Ulsan College of Medicine, Asan Medical Center , Seoul , South Korea
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Role of protein kinase D2 phosphorylation on Tyr in modulation by ghrelin of Helicobacter pylori-induced up-regulation in gastric mucosal matrix metalloproteinase-9 (MMP-9) secretion. Inflammopharmacology 2016; 24:119-26. [PMID: 27209313 DOI: 10.1007/s10787-016-0267-2] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/15/2016] [Accepted: 05/10/2016] [Indexed: 01/26/2023]
Abstract
Matrix metalloproteinas-9 (MMP-9) is a glycosylated endopeptidase associated with host reaction to microbial endotoxins and also characterizes gastric mucosal inflammatory response to H. pylori infection. Here, we report on the factors involved in gastric mucosal MMP-9 secretion in response to H. pylori LPS, and the effect of hormone, ghrelin. We show that both the LPS-elicited induction in MMP-9 secretion and also the modulatory influence of ghrelin occur at the level of MMP-9 processing between the endoplasmic reticulum (ER) and Golgi. Further, we demonstrate that the LPS effect is associated with up-regulation in the activation of Arf1, a small GTPase of the ADP-ribosylation factor family, and the recruitment and phosphorylation of protein kinase D2 (PKD2), involved in the secretory cargo processing in the Golgi. Moreover, we reveal that the LPS-induced up-regulation in MMP-9 secretion is reflected in a marked increase in PKCδ-mediated PKD2 phosphorylation on Ser, while the modulatory effect of ghrelin is manifested by the SFK-PTKs-dependent phosphorylation of PKD2 on Tyr. Thus, our findings demonstrate the role of Arf1/PKD2 in mediation of H. pylori LPS-induced up-regulation in gastric mucosal MMP-9 secretion and suggest the modulatory mechanism of ghrelin action.
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Regulatory role of guanine nucleotide exchange factor (GEF) Dock180 phosphorylation on Tyr/Ser in mediation of gastric mucosal Rac1 activation in response to Helicobacter pylori and ghrelin. Inflammopharmacology 2015; 23:111-8. [PMID: 25957600 DOI: 10.1007/s10787-015-0235-2] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/17/2015] [Accepted: 04/28/2015] [Indexed: 01/26/2023]
Abstract
A small GTPase, Rac1, is recognized as an important modulator of the inflammatory responses to bacterial lipopolysaccharide (LPS) by affecting the processes of phospholipase C activation. The activation of Rac1 involves the exchange of GDP for GTP and is catalyzed by the guanine nucleotide exchange factors (GEFs). Here, we report on the gastric mucosal GEF, Dock180, activation in response to H. pylori PS, and the hormone, ghrelin. We show that stimulation of gastric mucosal cells with the LPS leads to up-regulation in Dock180 phosphorylation on Tyr and Ser that is accompanied by a massive rise in Rac1-GTP level, while the effect of ghrelin, manifested by a drop in Dock180 phosphorylation on Ser, is associated with a decrease in Rac1-GTP formation. Furthermore, we demonstrate that phosphorylation on Tyr remains under the control of the Src family protein tyrosine kinases (SFK-PTKs), and is accompanied by Dock180 membrane translocation, while phosphorylation of the membrane-localized Dock180 on Ser represents the stimulatory contribution of protein kinase Cδ (PKCδ) to Dock180 activation. Moreover, we reveal that the interaction between Dock180 and PKCδ is dependent on Dock180 Tyr phosphorylation as well as the activity of PKCδ. Thus, our findings point to the involvement of PKCδ in the LPS-induced up-regulation of Dock180 activation, and suggest the modulatory mechanism of ghrelin influence on the gastric mucosal inflammatory responses to H. pylori.
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Slomiany BL, Slomiany A. Mechanism of Rac1-induced amplification in gastric mucosal phospholipase Cγ2 activation in response to Helicobacter pylori: modulatory effect of ghrelin. Inflammopharmacology 2015; 23:101-9. [PMID: 25796615 DOI: 10.1007/s10787-015-0231-6] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2015] [Accepted: 03/04/2015] [Indexed: 12/27/2022]
Abstract
Membrane recruitment followed by targeted phosphorylation of specific Tyr and Ser residues and the interaction with Rac GTPases are the crucial parts of an elaborate mechanism of PLCγ2 activation essential for its role in linking the specific receptor responses to a variety of hormones and bacterial endotoxins with the intended intracellular targets. Here, we explored the involvement of Rac in mediation of PLCγ2 activation associated with gastric mucosal inflammatory responses to H. pylori LPS and the hormone, ghrelin. We show that stimulation of gastric mucosal cells with the LPS leads to the membrane translocation of Rac1 as well as PLCγ2, while the effect of ghrelin is manifested by elevation in the membrane PLCγ2 activation and suppression in Rac1 translocation. However, blocking the LPS-induced Rac1 translocation, while detrimental to the PLCγ2 activation, has no effect on its membrane translocation. We reveal further that PLCγ2, localized in the membrane in association with Rac1 following the LPS stimulation, exhibits a marked increase in phosphorylation on Ser, while the modulatory effect of ghrelin, manifested by a drop in Rac1 translocation, is associated with a distinct decrease in PLCγ2 phosphorylation on Ser. Thus, the results suggest that H. pylori-elicited increase in gastric mucosal PLCγ2 phosphorylation on Ser serves as an essential platform for Rac1 colocalization and amplification in PLCγ2 activation.
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Affiliation(s)
- B L Slomiany
- Research Center C875, Rutgers School of Dental Medicine Rutgers, The State University of New Jersey, 110 Bergen Street, PO Box 1709, Newark, NJ, 07103-2400, USA,
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Tang J, Lin J. Relationship between ghrelin and gastrointestinal diseases. Shijie Huaren Xiaohua Zazhi 2014; 22:5447-5453. [DOI: 10.11569/wcjd.v22.i35.5447] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
Ghrelin is a newly found 28-amino acid brain-gut peptide, which is mainly secreted by the gastric mucosa. It has two forms, acyl-ghrelin and des-acyl ghrelin, and the former is the major active form. Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor and plays an important role in regulating food intake, gastric acid secretion, gastrointestinal motility, gastric mucosa protection, and inhibition of inflammatory reaction in paracrine, autocrine and endocrine manners. Recent studies have found that ghrelin levels are abnormal in a variety of gastrointestinal diseases, such as Helicobacter pylori infection, peptic ulcer, functional dyspepsia, inflammatory bowel disease, pancreatitis, tumors and so on, suggesting that ghrelin may be involved in the pathogenesis of these diseases. Ghrelin may become an index for disease diagnosis and prognosis evaluation and a new target for treatment of gastrointestinal diseases.
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Xu C, Yan M, Sun Y, Joo J, Wan X, Yu C, Wang Q, Shen C, Chen P, Li Y, Coleman WG. Prevalence of Helicobacter pylori infection and its relation with body mass index in a Chinese population. Helicobacter 2014; 19:437-42. [PMID: 25256639 DOI: 10.1111/hel.12153] [Citation(s) in RCA: 56] [Impact Index Per Article: 5.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND Helicobacter pylori infection is highly prevalent worldwide. The association between obesity and H. pylori infection is controversial in the literature. This study aims to investigate the prevalence of H. pylori infection and its relation with body mass index (BMI) in a Chinese population. MATERIALS AND METHODS A cross-sectional study was performed among adults who underwent health checkups at the First Affiliated Hospital, College of Medicine, Zhejiang University in 2013. The prevalence of H. pylori infection was examined by (13)C urea breath tests, and the association between prevalence of H. pylori infection and BMI was analyzed. RESULTS Of the 8820 participants enrolled, 3859 (43.8%) were positive for H. pylori infection. H. pylori-positive participants had a more unfavorable metabolic profile than H. pylori-negative participants. Overweight/obese participants showed a higher prevalence of H. pylori infection than that of lean participants, and a positive linear correlation between BMI and prevalence of H. pylori infection was observed. Both unadjusted and adjusted analysis revealed that BMI was significantly associated with risk factors of H. pylori infection. CONCLUSIONS Our results showed that BMI was significantly and positively associated with H. pylori infection, and a high BMI was associated with an increased risk of the infection.
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Affiliation(s)
- Chengfu Xu
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China; Cancer Cluster, National Institute on Minority Health and Health Disparities, National Institutes of Health, Bethesda, MD, USA; Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
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Role of amplification in phospholipase Cγ2 activation in modulation of gastric mucosal inflammatory responses to Helicobacter pylori: effect of ghrelin. Inflammopharmacology 2014; 23:37-45. [PMID: 25362585 DOI: 10.1007/s10787-014-0220-1] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/09/2014] [Accepted: 10/18/2014] [Indexed: 12/21/2022]
Abstract
Phosphoinositide-specific phospholipase C (PLC) enzymes are crucial elements of signal transduction pathways that provide a common link of communication integrating specific receptor responses to a variety of hormones, growth factors, and bacterial endotoxins with the intended intracellular targets. Here, we examined the involvement of PLC in modulation of gastric mucosal inflammatory responses to Helicobacter pylori LPS by peptide hormone, ghrelin. We show that stimulation of gastric mucosal cells with the LPS leads to the activation and membrane translocation of the γ2 isoform of PLC, phosphorylated on Tyr as well as Ser, while the effect of ghrelin is reflected in the translocation and phosphorylation of membrane-associated PLCγ2 on Tyr mainly. Moreover, we demonstrate that PLCγ2 phosphorylation on Tyr remains under the control of the Src family protein tyrosine kinases (SFK-PTKs), and is intimately linked to PLCγ2 membrane localization, while the LPS-induced phosphorylation of membrane-recruited PLCγ2 on Ser displays dependence on protein kinase Cδ (PKCδ) and leads to the amplification in PLCγ2 activation. Thus, our findings link the extent of H. pylori-elicited gastric mucosal inflammatory involvement to the PKCδ-mediated amplification in PLCγ2 activation through phosphorylation on Ser.
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