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For: Wang C, Guan Y, Yang J. Cytokines in the Progression of Pancreatic β-Cell Dysfunction. Int J Endocrinol 2010;2010:515136. [PMID: 21113299 PMCID: PMC2989452 DOI: 10.1155/2010/515136] [Citation(s) in RCA: 99] [Impact Index Per Article: 6.6] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/28/2010] [Revised: 08/05/2010] [Accepted: 10/07/2010] [Indexed: 12/29/2022] Open

For:	Wang C, Guan Y, Yang J. Cytokines in the Progression of Pancreatic β-Cell Dysfunction. Int J Endocrinol 2010;2010:515136. [PMID: 21113299 PMCID: PMC2989452 DOI: 10.1155/2010/515136] [Citation(s) in RCA: 99] [Impact Index Per Article: 6.6] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/28/2010] [Revised: 08/05/2010] [Accepted: 10/07/2010] [Indexed: 12/29/2022] Open

Number

Cited by Other Article(s)

Ajmal N, Bogart MC, Khan P, Max-Harry IM, Healy AM, Nunemaker CS. Identifying Promising Immunomodulators for Type 1 Diabetes (T1D) and Islet Transplantation. J Diabetes Res 2024;2024:5151171. [PMID: 39735417 PMCID: PMC11679277 DOI: 10.1155/jdr/5151171] [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: 09/08/2024] [Accepted: 12/04/2024] [Indexed: 12/31/2024] Open

Abstract

Type 1 diabetes (T1D) is an autoimmune chronic disorder that damages beta cells in the pancreatic islets of Langerhans and results in hyperglycemia due to the loss of insulin. Exogenous insulin therapy can save lives but does not stop disease progression. Thus, an effective therapy may require beta cell restoration and suppression of the autoimmune response. However, currently, there are no treatment options available that can reverse T1D. Within the National Clinical Trial (NCT) database, a majority of over 3000 trials to treat T1D are devoted to insulin therapy. This review focuses on noninsulin pharmacological therapies, specifically immunomodulators. Many investigational new drugs fall under this category, such as the recently FDA-approved CD3 monoclonal antibody teplizumab to delay the onset of T1D. In total, we identified 39 different immunomodulatory investigational drugs. FDA-approved teplizumab for Stage 2 T1D is discussed along with other immunomodulators that have been tested in Phase 3 clinical trials or higher, including otelixizumab (another anti-CD3 monoclonal antibody), daclizumab (an anti-CD25 monoclonal antibody), ladarixin (CXCR1/2 inhibitor), and antithymocyte globulin (ATG). Immunomodulators also play roles in islet transplantation and cellular therapies like FDA-approved Lantidra. Several immunomodulators involved in Phase 3 clinical studies of islet transplantation are also discussed, including alemtuzumab, basiliximab, etanercept, and reparixin, some already FDA-approved for other uses. These include alemtuzumab, basiliximab, etanercept, and reparixin, some of which have been FDA-approved for other uses. This review provides background, mechanism of action, results of completed trials, and adverse effects as well as details regarding ongoing clinical trials for each of these immunomodulators. Trial Registration: ClinicalTrials.gov identifier: NCT03875729, NCT01030861, NCT00129259, NCT00385697, NCT01280682; NCT03929601, NCT04598893, NCT05757713, NCT00678886, NCT01123083, NCT00064714, NCT00468117, NCT04628481, NCT01106157, NCT02215200, NCT00331162, NCT00679042, NCT01220856, NCT01817959.

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Wang J, Shen Y, Chen H, Guan J, Li Z, Liu X, Guo S, Wang L, Yan B, Jin C, Li H, Guo T, Sun Y, Zhang W, Zhang Z, Tian Y, Tian Z. Non-lethal sonodynamic therapy inhibits high glucose and palmitate-induced macrophage inflammasome activation through mtROS-DRP1-mitophagy pathway. FASEB J 2024;38:e70178. [PMID: 39556373 DOI: 10.1096/fj.202402008r] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/28/2024] [Revised: 10/18/2024] [Accepted: 11/01/2024] [Indexed: 11/19/2024]

Affiliation(s)

Jiayu Wang Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Yicheng Shen Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Heyu Chen Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Jinwei Guan Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Zhitao Li Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Xianna Liu Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Shuyuan Guo Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China Department of Cardiology, 1st Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, P. R. China
Linxin Wang Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China Department of Cardiology, 1st Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, P. R. China
Baoyue Yan Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Chenrun Jin Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
He Li Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Tian Guo Medical College of Jining Medical University, Jining, P. R. China
Yun Sun Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Weihua Zhang Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China
Zhiguo Zhang School of Physics, Harbin Institute of Technology, Harbin, P. R. China School of Instrumentation Science and Engineering, Harbin Institute of Technology, Harbin, P. R. China
Ye Tian Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China Department of Cardiology, 1st Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, P. R. China
Zhen Tian Department of Pathophysiology, Harbin Medical University, Harbin, P. R. China Key Laboratory of Acoustic, Optical, Electrical and Magnetic Diagnostics and Treatment of Cardiovascular Diseases in Heilongjiang Province, Harbin, P. R. China

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Ergul Erkec O, Huyut Z, Acikgoz E, Huyut MT. Effects of exogenous ghrelin treatment on oxidative stress, inflammation and histological parameters in a fat-fed streptozotocin rat model. Arch Physiol Biochem 2024:1-11. [PMID: 39324977 DOI: 10.1080/13813455.2024.2407551] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/16/2024] [Revised: 07/17/2024] [Accepted: 09/16/2024] [Indexed: 09/27/2024]

Negi V, Lee J, Mandi V, Danvers J, Liu R, Perez-Garcia EM, Li F, Jagannathan R, Yang P, Filingeri D, Kumar A, Ma K, Moulik M, Yechoor VK. Bromodomain Protein Inhibition Protects β-Cells from Cytokine-Induced Death and Dysfunction via Antagonism of NF-κB Pathway. Cells 2024;13:1108. [PMID: 38994961 PMCID: PMC11240345 DOI: 10.3390/cells13131108] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/25/2024] [Revised: 06/10/2024] [Accepted: 06/18/2024] [Indexed: 07/13/2024] Open

Affiliation(s)

Vinny Negi Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Jeongkyung Lee Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Varun Mandi Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Joseph Danvers Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Ruya Liu Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Eliana M. Perez-Garcia Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Feng Li Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Rajaganapati Jagannathan Division of Cardiology, Department of Pediatrics, Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA 15224, USA; (R.J.); (M.M.)
Ping Yang Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Domenic Filingeri Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Amit Kumar Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)
Ke Ma Department of Diabetes Complications and Metabolism, Diabetes and Metabolism Research Institute, City of Hope National Medical Center, Duarte, CA 91010, USA;
Mousumi Moulik Division of Cardiology, Department of Pediatrics, Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA 15224, USA; (R.J.); (M.M.)
Vijay K. Yechoor Diabetes and Beta Cell Biology Center, Division of Endocrinology and Metabolism, University of Pittsburgh, Pittsburgh, PA 15213, USA; (V.N.); (J.L.); (V.M.); (R.L.); (E.M.P.-G.); (F.L.); (D.F.); (A.K.)

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Arefanian H, Al Madhoun A, Al-Rashed F, Alzaid F, Bahman F, Nizam R, Alhusayan M, John S, Jacob S, Williams MR, Abukhalaf N, Shenouda S, Joseph S, AlSaeed H, Kochumon S, Mohammad A, Koti L, Sindhu S, Abu-Farha M, Abubaker J, Thanaraj TA, Ahmad R, Al-Mulla F. Unraveling Verapamil's Multidimensional Role in Diabetes Therapy: From β-Cell Regeneration to Cholecystokinin Induction in Zebrafish and MIN6 Cell-Line Models. Cells 2024;13:949. [PMID: 38891081 PMCID: PMC11171639 DOI: 10.3390/cells13110949] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/27/2024] [Revised: 05/15/2024] [Accepted: 05/24/2024] [Indexed: 06/21/2024] Open

Affiliation(s)

Hossein Arefanian Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.)
Ashraf Al Madhoun Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.A.M.); (R.N.); (S.J.); (S.J.); (L.K.); (T.A.T.) Animal and Imaging Core Facility, Dasman Diabetes Institute, Dasman 15462, Kuwait;
Fatema Al-Rashed Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.)
Fawaz Alzaid Department of Bioenergetics & Neurometabolism, Dasman Diabetes Institute, Dasman 15462, Kuwait; (F.A.); (M.A.); (M.R.W.) Institut Necker Enfants Malades (INEM), French Institute of Health and Medical Research (INSERM), Immunity & Metabolism of Diabetes (IMMEDIAB), Université de Paris Cité, 75014 Paris, France
Fatemah Bahman Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.)
Rasheeba Nizam Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.A.M.); (R.N.); (S.J.); (S.J.); (L.K.); (T.A.T.)
Mohammed Alhusayan Department of Bioenergetics & Neurometabolism, Dasman Diabetes Institute, Dasman 15462, Kuwait; (F.A.); (M.A.); (M.R.W.)
Sumi John Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.A.M.); (R.N.); (S.J.); (S.J.); (L.K.); (T.A.T.)
Sindhu Jacob Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.A.M.); (R.N.); (S.J.); (S.J.); (L.K.); (T.A.T.)
Michayla R. Williams Department of Bioenergetics & Neurometabolism, Dasman Diabetes Institute, Dasman 15462, Kuwait; (F.A.); (M.A.); (M.R.W.)
Nermeen Abukhalaf Animal and Imaging Core Facility, Dasman Diabetes Institute, Dasman 15462, Kuwait;
Steve Shenouda Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.)
Shibu Joseph Special Services Facilities, Dasman Diabetes Institute, Dasman 15462, Kuwait;
Halemah AlSaeed Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.)
Shihab Kochumon Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.)
Anwar Mohammad Department of Biochemistry and Molecular Biology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.M.); (M.A.-F.); (J.A.)
Lubaina Koti Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.A.M.); (R.N.); (S.J.); (S.J.); (L.K.); (T.A.T.)
Sardar Sindhu Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.) Animal and Imaging Core Facility, Dasman Diabetes Institute, Dasman 15462, Kuwait;
Mohamed Abu-Farha Department of Biochemistry and Molecular Biology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.M.); (M.A.-F.); (J.A.) Department of Translational Research, Dasman Diabetes Institute, Dasman 15462, Kuwait
Jehad Abubaker Department of Biochemistry and Molecular Biology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.M.); (M.A.-F.); (J.A.)
Thangavel Alphonse Thanaraj Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.A.M.); (R.N.); (S.J.); (S.J.); (L.K.); (T.A.T.)
Rasheed Ahmad Department of Immunology & Microbiology, Dasman Diabetes Institute, Dasman 15462, Kuwait; (H.A.); (F.A.-R.); (F.B.); (S.S.); (H.A.); (S.K.); (S.S.); (R.A.)
Fahd Al-Mulla Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15462, Kuwait; (A.A.M.); (R.N.); (S.J.); (S.J.); (L.K.); (T.A.T.)

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Han HW, Pradhan G, Villarreal D, Kim DM, Jain A, Gaharwar A, Tian Y, Guo S, Sun Y. GHSR Deletion in β-Cells of Male Mice: Ineffective in Obesity, but Effective in Protecting against Streptozotocin-Induced β-Cell Injury in Aging. Nutrients 2024;16:1464. [PMID: 38794702 PMCID: PMC11123813 DOI: 10.3390/nu16101464] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/15/2024] [Revised: 05/09/2024] [Accepted: 05/10/2024] [Indexed: 05/26/2024] Open

Martínez-Esquivias F, Perez-Larios A, Guzmán-Flores JM. Effect of Administration of Selenium Nanoparticles Synthesized Using Onion Extract on Biochemical and Inflammatory Parameters in Mice Fed with High-Fructose Diet: In Vivo and In Silico Analysis. Biol Trace Elem Res 2024;202:558-568. [PMID: 37119340 DOI: 10.1007/s12011-023-03685-1] [Citation(s) in RCA: 4] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/23/2023] [Accepted: 04/26/2023] [Indexed: 05/01/2023]

Abdel-Moneim A, Mahmoud R, Allam G, Mahmoud B. Relationship between Cytokines and Metabolic Syndrome Components: Role of Pancreatic-Derived Factor, Interleukin-37, and Tumor Necrosis Factor-α in Metabolic Syndrome Patients. Indian J Clin Biochem 2024;39:37-46. [PMID: 38223016 PMCID: PMC10784435 DOI: 10.1007/s12291-022-01079-z] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/07/2022] [Accepted: 07/21/2022] [Indexed: 10/14/2022]

Yoopum S, Wongmanee N, Rojanaverawong W, Rattanapunya S, Sumsakul W, Hanchang W. Mango (Mangifera indica L.) seed kernel extract suppresses hyperglycemia by modulating pancreatic β cell apoptosis and dysfunction and hepatic glucose metabolism in diabetic rats. ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH INTERNATIONAL 2023;30:123286-123308. [PMID: 37981611 DOI: 10.1007/s11356-023-31066-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/14/2023] [Accepted: 11/12/2023] [Indexed: 11/21/2023]

Abstract

This study investigated the anti-hyperglycemic action of mango seed kernel extract (MKE) and various mechanisms involved in its actions to improve pancreatic β cells and hepatic carbohydrate metabolism in diabetic rats. An intraperitoneal injection of 60 mg/kg of streptozotocin (STZ) followed by 30 consecutive days of treatment with MKE (250, 500, and 1000 mg/kg body weight) was used to establish a study group of diabetic rats. Using liquid chromatography-electrospray ionization-quadrupole time-of-flight mass spectrometry (LC-ESI-QTOF-MS/MS) for identification, 26 chemical compounds were found in MKE and the high-performance liquid chromatography (HPLC) analysis of the MKE also revealed the existence of mangiferin, gallic acid, and quercetin. The results confirmed that in each diabetes-affected rat, MKE mitigated the heightened levels of fasting blood glucose, diabetic symptoms, glucose intolerance, total cholesterol (TC), and low-density lipoprotein-cholesterol (LDL-C). As demonstrated by a remarkable increment in serum and pancreatic insulin, the diabetic pancreatic β cell function was potentiated by treating with MKE. The effect of MKE on diabetic pancreatic apoptosis clearly reduced the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells, which was related to diminished levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and Bax and an increase in Bcl-xL protein expression. Furthermore, diabetes-induced liver damage was clearly ameliorated along with a notable reduction in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and abnormal liver histology. By enhancing anti-oxidant superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, MKE alleviated diabetes-induced pancreatic and liver oxidative damage, as demonstrated by diminished levels of malondialdehyde. In minimizing the expression levels of glucose 6-phosphatase and phosphoenolpyruvate carboxykinase-1 proteins in the diabetic liver, MKE also enhanced glycogen content and hexokinase activity. Collectively, these findings indicate that by suppressing oxidative and inflammatory processes, MKE exerts a potent anti-hyperglycemic activity in diabetic rats which serve to protect pancreatic β cell apoptosis, enhance their function, and improve hepatic glucose metabolism.

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Sionov RV, Ahdut-HaCohen R. A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome. Biomedicines 2023;11:2558. [PMID: 37761001 PMCID: PMC10527322 DOI: 10.3390/biomedicines11092558] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/15/2023] [Revised: 09/06/2023] [Accepted: 09/14/2023] [Indexed: 09/29/2023] Open

Camaya I, O’Brien B, Donnelly S. How do parasitic worms prevent diabetes? An exploration of their influence on macrophage and β-cell crosstalk. Front Endocrinol (Lausanne) 2023;14:1205219. [PMID: 37564976 PMCID: PMC10411736 DOI: 10.3389/fendo.2023.1205219] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/13/2023] [Accepted: 07/10/2023] [Indexed: 08/12/2023] Open

Abstract

Diabetes is the fastest growing chronic disease globally, with prevalence increasing at a faster rate than heart disease and cancer. While the disease presents clinically as chronic hyperglycaemia, two distinct subtypes have been recognised. Type 1 diabetes (T1D) is characterised as an autoimmune disease in which the insulin-producing pancreatic β-cells are destroyed, and type 2 diabetes (T2D) arises due to metabolic insufficiency, in which inadequate amounts of insulin are produced, and/or the actions of insulin are diminished. It is now apparent that pro-inflammatory responses cause a loss of functional β-cell mass, and this is the common underlying mechanism of both T1D and T2D. Macrophages are the central immune cells in the pathogenesis of both diseases and play a major role in the initiation and perpetuation of the proinflammatory responses that compromise β-cell function. Furthermore, it is the crosstalk between macrophages and β-cells that orchestrates the inflammatory response and ensuing β-cell dysfunction/destruction. Conversely, this crosstalk can induce immune tolerance and preservation of β-cell mass and function. Thus, specifically targeting the intercellular communication between macrophages and β-cells offers a unique strategy to prevent/halt the islet inflammatory events underpinning T1D and T2D. Due to their potent ability to regulate mammalian immune responses, parasitic worms (helminths), and their excretory/secretory products, have been examined for their potential as therapeutic agents for both T1D and T2D. This research has yielded positive results in disease prevention, both clinically and in animal models. However, the focus of research has been on the modulation of immune cells and their effectors. This approach has ignored the direct effects of helminths and their products on β-cells, and the modulation of signal exchange between macrophages and β-cells. This review explores how the alterations to macrophages induced by helminths, and their products, influence the crosstalk with β-cells to promote their function and survival. In addition, the evidence that parasite-derived products interact directly with endocrine cells to influence their communication with macrophages to prevent β-cell death and enhance function is discussed. This new paradigm of two-way metabolic conversations between endocrine cells and macrophages opens new avenues for the treatment of immune-mediated metabolic disease.

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Singh A, Afshan N, Singh A, Singh SK, Yadav S, Kumar M, Sarma DK, Verma V. Recent trends and advances in type 1 diabetes therapeutics: A comprehensive review. Eur J Cell Biol 2023;102:151329. [PMID: 37295265 DOI: 10.1016/j.ejcb.2023.151329] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2023] [Revised: 05/12/2023] [Accepted: 06/03/2023] [Indexed: 06/12/2023] Open

Prentice B, Nicholson M, Lam GY. Cystic fibrosis related diabetes (CFRD) in the era of modulators: A scoping review. Paediatr Respir Rev 2023;46:23-29. [PMID: 36581478 DOI: 10.1016/j.prrv.2022.11.005] [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: 08/24/2022] [Accepted: 11/30/2022] [Indexed: 12/12/2022]

Ge Y, Bruno M, Nash MS, Coates NH, Chorley BN, Cave MC, Beier JI. Vinyl chloride enhances high-fat diet-induced proteome alterations in the mouse pancreas related to metabolic dysfunction. Toxicol Sci 2023;193:103-114. [PMID: 36892438 PMCID: PMC10176240 DOI: 10.1093/toxsci/kfad024] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 03/10/2023] Open

Ademola SA, Bamikole OJ, Amodu OK. Is TNF alpha a mediator in the co-existence of malaria and type 2 diabetes in a malaria endemic population? Front Immunol 2023;14:1028303. [PMID: 37215099 PMCID: PMC10196125 DOI: 10.3389/fimmu.2023.1028303] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/25/2022] [Accepted: 04/25/2023] [Indexed: 05/24/2023] Open

Abstract

Malaria remains a disease of public health importance globally, especially in sub-Saharan Africa. Malaria deaths reduced globally steadily between 2000-2019, however there was a 10% increase in 2020 due to disruptions in medical service during the COVID-19 pandemic. Globally, about 96% of malaria deaths occurred in 29 countries; out of which, four countries (Nigeria, the Democratic Republic of the Congo, the Niger, and the United Republic of Tanzania) accounted for just over half of the malaria deaths. Nigeria leads the four countries with the highest malaria deaths (accounting for 31% globally). Parallelly, sub-Saharan Africa is faced with a rise in the incidence of Type 2 diabetes (T2D). Until recently, T2D was a disease of adulthood and old age. However, this is changing as T2D in children and adolescents is becoming an increasingly important public health problem. Nigeria has been reported to have the highest burden of diabetes in Africa with a prevalence of 5.77% in the country. Several studies conducted in the last decade investigating the interaction between malaria and T2D in developing countries have led to the emergence of the intra-uterine hypothesis. The hypothesis has arisen as a possible explanation for the rise of T2D in malaria endemic areas; malaria in pregnancy could lead to intra-uterine stress which could contribute to low birth weight and may be a potential cause of T2D later in life. Hence, previous, and continuous exposure to malaria infection leads to a higher risk of T2D. Current and emerging evidence suggests that an inflammation-mediated link exists between malaria and eventual T2D emergence. The inflammatory process thus, is an important link for the co-existence of malaria and T2D because these two diseases are inflammatory-related. A key feature of T2D is systemic inflammation, characterized by the upregulation of inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) which leads to impaired insulin signaling. Malaria infection is an inflammatory disease in which TNF-α also plays a major role. TNF-α plays an important role in the pathogenesis and development of malaria and T2D. We therefore hypothesize that TNF-α is an important link in the increasing co-existence of T2D.

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Dludla PV, Mabhida SE, Ziqubu K, Nkambule BB, Mazibuko-Mbeje SE, Hanser S, Basson AK, Pheiffer C, Kengne AP. Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress. World J Diabetes 2023;14:130-146. [PMID: 37035220 PMCID: PMC10075035 DOI: 10.4239/wjd.v14.i3.130] [Citation(s) in RCA: 65] [Impact Index Per Article: 32.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/12/2022] [Revised: 11/26/2022] [Accepted: 02/28/2023] [Indexed: 03/15/2023] Open

The role of cytokines and T-bet, GATA3, ROR-γt, and FOXP3 transcription factors of T cell subsets in the natural clinical progression of Type 1 Diabetes. Immunol Res 2023;71:451-462. [PMID: 36595206 DOI: 10.1007/s12026-022-09355-z] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/17/2022] [Accepted: 12/26/2022] [Indexed: 01/04/2023]

Hanchang W, Wongmanee N, Yoopum S, Rojanaverawong W. Protective role of hesperidin against diabetes induced spleen damage: Mechanism associated with oxidative stress and inflammation. J Food Biochem 2022;46:e14444. [PMID: 36165434 DOI: 10.1111/jfbc.14444] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/06/2022] [Revised: 08/21/2022] [Accepted: 09/16/2022] [Indexed: 01/14/2023]

Abstract

Diabetes mellitus is a metabolic disease affecting various organs, including the spleen and is characterized by chronic hyperglycemia. Oxidative and inflammatory stress are key mediators in the development of spleen damage caused by diabetes. This study aimed to examine the splenoprotective effect of hesperidin and the mechanisms underlying its capacity to reduce oxidative stress and inflammation-mediated spleen damage in diabetes. The diabetic rats used in this study were induced with a 65 mg per kg body weight of streptozotocin. This was followed by 4 weeks of continuous daily dosage of hesperidin treatment at 100 mg/kg body weight. The results showed that hesperidin improved spleen weight and histopathological alterations in the diabetic rats. The hesperidin-treated diabetic group showed a marked induction of SOD and GPx enzymes and moderated malondialdehyde level. This was in addition to an obvious decrease in the levels of TNF-α and NF-ᴋB in the diabetic rat spleen. Through a remarkable upregulation in Bcl-xL and downregulation in Bax and cleaved caspase-3 proteins, hesperidin supplementation rescued splenic cell apoptosis in the diabetic rats. These findings demonstrate the effectiveness of hesperidin in helping regulate Bcl-2 family proteins and inhibiting the oxidative stress and inflammatory status of hyperglycemia-mediated spleen apoptosis. PRACTICAL APPLICATIONS: Diabetes-related spleen damage increases immune dysfunction, which often results in the heightened risks of infection, morbidity and mortality in diabetic patients. In this work, hesperidin was used in the treatment of rats with diabetes-induced splenic damage. The results were highly encouraging with hesperidin consistently presenting beneficial antioxidant and anti-inflammatory qualities and splenoprotective effect. Research outcomes support the notion that hesperidin treatment could be considered a good strategy for the prevention of diabetic complications in the spleen.

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Tang X. The risk of organ-based comorbidities in psoriasis: a systematic review and meta-analysis. An Bras Dermatol 2022;97:612-623. [PMID: 35850940 PMCID: PMC9453528 DOI: 10.1016/j.abd.2021.10.007] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/05/2021] [Revised: 09/30/2021] [Accepted: 10/04/2021] [Indexed: 02/06/2023] Open

Abstract

Background

The close relationship between psoriasis and concomitant diseases is widely accepted. However, a comprehensive analysis of organ-based comorbidities in psoriasis is still lacking.

Objective

The authors aimed to present the risk of organ-based comorbidities in psoriasis by comparing the general population.

Methods

The authors retrieved a search of Pubmed, EMBASE, and Cochrane databases for studies reporting organ-based comorbidities in psoriasis versus the general population. Observational studies that met the following criteria were assessed: 1) Psoriasis diagnosis; 2) Cardiovascular or kidney or liver or respiratory or cerebrovascular outcomes; 3) Comparison group of individuals without psoriasis. Pooled Relative Risks (pRRs) and 95% Confidence Intervals (CIs) were calculated by using the random-effect model.

Results

Fifteen observational studies with 216,348 psoriatic patients and 9,896,962 individuals from the general population were included. Psoriasis showed a greater risk of organ-based comorbidities. Compared to the general population, pRR for all organ-based comorbidities was 1.20 (95% CI 1.11‒1.31) in psoriasis, and pRR was lower in mild 0.61 (95% CI 0.46‒0.81) than in moderate/severe patients. pRR was 1.20 (95% CI 1.11‒1.30) for cardiovascular, 1.56 (95% CI 1.20‒2.04), and 1.75 (95% CI 1.33‒2.29) for cerebrovascular and liver diseases, respectively. pRR for coexisting renal and cardiovascular events was 1.09 (95% CI 1.01‒1.18). pRR for coexisting renal and cerebrovascular events was 1.28 (95% CI 0.99‒1.66). pRR for coexisting renal and liver diseases was 1.46 (95% CI 1.10‒1.94). pRR for coexisting cardiovascular and liver diseases was 1.41 (95% CI 1.11‒1.80).

Study limitations

There is heterogeneity.

Conclusion

Psoriasis has a higher risk of single and multiple organ-based comorbidities than the general population. The present study will further improve attention to psoriasis as a systemic inflammatory disease.

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Qin T, Hu S, Smink AM, de Haan BJ, Silva-Lagos LA, Lakey JR, de Vos P. Inclusion of extracellular matrix molecules and necrostatin-1 in the intracapsular environment of alginate-based microcapsules synergistically protects pancreatic β cells against cytokine-induced inflammatory stress. Acta Biomater 2022;146:434-449. [PMID: 35500812 DOI: 10.1016/j.actbio.2022.04.042] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/25/2022] [Revised: 04/22/2022] [Accepted: 04/26/2022] [Indexed: 11/01/2022]

Abstract

Immunoisolation of pancreatic islets in alginate-based microcapsules is a promising approach for grafting of islets in absence of immunosuppression. However, loss and damage to the extracellular matrix (ECM) during islet isolation enhance susceptibility of islets for inflammatory stress. In this study, a combined strategy was applied to reduce this stress by incorporating ECM components (collagen type IV/RGD) and necroptosis inhibitor, necrostatin-1 (Nec-1) in alginate-based microcapsules in vitro. To demonstrate efficacy, viability and function of MIN6 β-cells and human islets in capsules with collagen type IV/RGD and/or Nec-1 was investigated in presence and absence of IL-1β, IFN-γ and TNF-α. The combination of collagen type IV/RGD and Nec-1 had higher protective effects than the molecules alone. Presence of collagen type IV/RGD and Nec-1 in the intracapsular environment reduced cytokine-induced overproduction of free radical species and unfavorable shifts in mitochondrial dynamics. In addition, the ECM components collagen type IV/RGD prevented a cytokine induced suppression of the FAK/Akt pathway. Our data indicate that the inclusion of collagen type IV/RGD and Nec-1 in the intracapsular environment prevents islet-cell loss when exposed to inflammatory stress, which might contribute to higher survival of β-cells in the immediate period after transplantation. This approach of inclusion of stress reducing agents in the intracapsular environment of immunoisolating devices may be an effective way to enhance the longevity of encapsulated islet grafts. STATEMENT OF SIGNIFICANCE: Islet-cells in immunoisolated alginate-based microcapsules are very susceptible to inflammatory stress which impacts long-term survival of islet grafts. Here we show that incorporation of ECM components (collagen type IV/RGD) and necrostatin-1 (Nec-1) in the intracapsular environment of alginate-based capsules attenuates this susceptibility and promotes islet-cell survival. This effect induced by collagen type IV/RGD and Nec-1 was probably due to lowering free radical production, preventing mitochondrial dysfunction and by maintaining ECM/integrin/FAK/Akt signaling and Nec-1/RIP1/RIP3 signaling. Our study provides an effective strategy to extend longevity of islet grafts which might be of great potential for future clinical application of immunoisolated cells.

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Farnsworth NL, Piscopio RA, Schleicher WE, Ramirez DG, Miranda JG, Benninger RKP. Modulation of Gap Junction Coupling Within the Islet of Langerhans During the Development of Type 1 Diabetes. Front Physiol 2022;13:913611. [PMID: 35837011 PMCID: PMC9274093 DOI: 10.3389/fphys.2022.913611] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2022] [Accepted: 06/09/2022] [Indexed: 01/07/2023] Open

Abstract

In type 1 diabetes (T1D), islet dysfunction occurs prior to diabetes onset. Pro-inflammatory cytokines can disrupt insulin secretion and Ca²⁺ homeostasis. Connexin36 (Cx36) gap junctions electrically couple β-cells to coordinate glucose-stimulated Ca²⁺ and insulin secretion. Cx36 gap junction coupling can also protect against cytokine-induced apoptosis. Our goal was to determine how islet gap junction coupling and Ca²⁺ dynamics are altered in mouse models of T1D prior to diabetes. Glucose tolerance was assessed in NOD and immunodeficient NOD-RAG1KO mice at 6-12 weeks age. Glucose-stimulated insulin secretion, Ca²⁺ dynamics, and gap junction coupling were measured in islets isolated at each age. Gap junction coupling was also measured in islets from mice that underwent transfer of diabetogenic splenocytes and from chromograninA knockout NOD mice. Cell death was measured in islets isolated from wild-type, Cx36 knockout or Cx36 over-expression mice, each treated with a cocktail of pro-inflammatory cytokines and K_ATP or SERCA activators/inhibitors. NOD mice over-expressing Cx36 were also monitored for diabetes development, and islets assessed for insulitis and apoptosis. NOD and NOD-RAG1KO controls showed similar glucose tolerance at all ages. Ca²⁺ dynamics and gap junction coupling were disrupted in islets of NOD mice at 9 weeks, compared to controls. Transfer of diabetogenic splenocytes also decreased gap junction coupling. Islets from chromograninA knockout mice displayed normal coupling. Overexpression of Cx36 protected islets from cytokine-induced apoptosis. A knockout of Cx36 amplified cytokine-induced apoptosis, which was reversed by K_ATP activation or SERCA activation. Cx36 overexpression in NOD mice delayed diabetes development compared to NOD controls. However, apoptosis and insulitis were not improved. Decreases in islet gap junction coupling occur prior to T1D onset. Such decreases alter islet susceptibility to apoptosis due to altered Ca²⁺. Future studies will determine if increasing Cx36 gap junction coupling in combination with restoring Ca²⁺ homeostasis protects against islet decline in T1D.

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Li J, Yan H, Xiang R, Yang W, Ye J, Yin R, Yang J, Chi Y. ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism. Front Physiol 2022;13:918042. [PMID: 35800345 PMCID: PMC9253475 DOI: 10.3389/fphys.2022.918042] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/12/2022] [Accepted: 05/30/2022] [Indexed: 11/13/2022] Open

Farhadnejad H, Teymoori F, Mokhtari E, Mirmiran P, Azizi F. Higher scores of dietary and lifestyle inflammatory indices are associated with increased risk of insulin-related disorders in Iranian adults. Eur J Clin Nutr 2022;76:1566-1575. [PMID: 35444270 DOI: 10.1038/s41430-022-01143-0] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/03/2021] [Revised: 03/29/2022] [Accepted: 04/04/2022] [Indexed: 11/09/2022]

Kannan P, Karthikeyan P, Subramaniam N, Mohan T, Gopinath B, Chakrapani LN, Palanivelu S, Raghunathan M, Periandavan K. Gymnemic acid protects murine pancreatic β-cells by moderating hyperglycemic stress-induced inflammation and apoptosis in type 1 diabetic rats. J Biochem Mol Toxicol 2022;36:e23050. [PMID: 35343011 DOI: 10.1002/jbt.23050] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/14/2021] [Revised: 02/02/2022] [Accepted: 03/10/2022] [Indexed: 11/08/2022]

ArefNezhad R, Motedayyen H, Roghani-Shahraki H. Do cytokines associate periodontitis with metabolic disorders? An overview of current documents. Endocr Metab Immune Disord Drug Targets 2022;22:778-786. [PMID: 35043774 DOI: 10.2174/1871530322666220119112026] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/04/2021] [Revised: 10/28/2021] [Accepted: 11/26/2021] [Indexed: 11/22/2022]

Bartolomé A. Stem Cell-Derived β Cells: A Versatile Research Platform to Interrogate the Genetic Basis of β Cell Dysfunction. Int J Mol Sci 2022;23:501. [PMID: 35008927 PMCID: PMC8745644 DOI: 10.3390/ijms23010501] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/02/2021] [Revised: 12/27/2021] [Accepted: 12/29/2021] [Indexed: 02/07/2023] Open

López-Bermudo L, Luque-Sierra A, Maya-Miles D, Gallego-Durán R, Ampuero J, Romero-Gómez M, Berná G, Martín F. Contribution of Liver and Pancreatic Islet Crosstalk to β-Cell Function/Dysfunction in the Presence of Fatty Liver. Front Endocrinol (Lausanne) 2022;13:892672. [PMID: 35651973 PMCID: PMC9148952 DOI: 10.3389/fendo.2022.892672] [Citation(s) in RCA: 10] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/09/2022] [Accepted: 04/12/2022] [Indexed: 11/13/2022] Open

Affiliation(s)

Lucía López-Bermudo Andalusian Center of Molecular Biology and Regenerative Medicine (CABIMER), University Pablo Olavide, University of Seville, CSIC, Seville, Spain Biomedical Research Network on Diabetes and Related Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain
Amparo Luque-Sierra Andalusian Center of Molecular Biology and Regenerative Medicine (CABIMER), University Pablo Olavide, University of Seville, CSIC, Seville, Spain
Douglas Maya-Miles Hospital Universitario Virgen del Rocío de Sevilla, Instituto de Biomedicina de Sevilla, Universidad de Sevilla, Sevilla, Spain Biomedical Research Network on Hepatic and Digestive Diseases (CIBEREHD), Instituto de Salud Carlos III, Madrid, Spain
Rocío Gallego-Durán Hospital Universitario Virgen del Rocío de Sevilla, Instituto de Biomedicina de Sevilla, Universidad de Sevilla, Sevilla, Spain Biomedical Research Network on Hepatic and Digestive Diseases (CIBEREHD), Instituto de Salud Carlos III, Madrid, Spain
Javier Ampuero Hospital Universitario Virgen del Rocío de Sevilla, Instituto de Biomedicina de Sevilla, Universidad de Sevilla, Sevilla, Spain Biomedical Research Network on Hepatic and Digestive Diseases (CIBEREHD), Instituto de Salud Carlos III, Madrid, Spain
Manuel Romero-Gómez Hospital Universitario Virgen del Rocío de Sevilla, Instituto de Biomedicina de Sevilla, Universidad de Sevilla, Sevilla, Spain Biomedical Research Network on Hepatic and Digestive Diseases (CIBEREHD), Instituto de Salud Carlos III, Madrid, Spain
Genoveva Berná Andalusian Center of Molecular Biology and Regenerative Medicine (CABIMER), University Pablo Olavide, University of Seville, CSIC, Seville, Spain Biomedical Research Network on Diabetes and Related Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain *Correspondence: Franz Martín, ; Genoveva Berná,
Franz Martín Andalusian Center of Molecular Biology and Regenerative Medicine (CABIMER), University Pablo Olavide, University of Seville, CSIC, Seville, Spain Biomedical Research Network on Diabetes and Related Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain *Correspondence: Franz Martín, ; Genoveva Berná,

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Dinić S, Arambašić Jovanović J, Uskoković A, Mihailović M, Grdović N, Tolić A, Rajić J, Đorđević M, Vidaković M. Oxidative stress-mediated beta cell death and dysfunction as a target for diabetes management. Front Endocrinol (Lausanne) 2022;13:1006376. [PMID: 36246880 PMCID: PMC9554708 DOI: 10.3389/fendo.2022.1006376] [Citation(s) in RCA: 38] [Impact Index Per Article: 12.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/29/2022] [Accepted: 09/05/2022] [Indexed: 11/14/2022] Open

Al-Selwi Y, Shaw JA, Kattner N. Understanding the Pancreatic Islet Microenvironment in Cystic Fibrosis and the Extrinsic Pathways Leading to Cystic Fibrosis Related Diabetes. CLINICAL MEDICINE INSIGHTS-ENDOCRINOLOGY AND DIABETES 2021;14:11795514211048813. [PMID: 34675737 PMCID: PMC8524685 DOI: 10.1177/11795514211048813] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 04/30/2021] [Accepted: 07/23/2021] [Indexed: 11/16/2022]

Naomi R, Bahari H, Yazid MD, Othman F, Zakaria ZA, Hussain MK. Potential Effects of Sweet Potato (Ipomoea batatas) in Hyperglycemia and Dyslipidemia-A Systematic Review in Diabetic Retinopathy Context. Int J Mol Sci 2021;22:10816. [PMID: 34639164 PMCID: PMC8509747 DOI: 10.3390/ijms221910816] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/07/2021] [Revised: 08/29/2021] [Accepted: 09/06/2021] [Indexed: 12/15/2022] Open

Abstract

Hyperglycemia is a condition with high glucose levels that may result in dyslipidemia. In severe cases, this alteration may lead to diabetic retinopathy. Numerous drugs have been approved by officials to treat these conditions, but usage of any synthetic drugs in the long term will result in unavoidable side effects such as kidney failure. Therefore, more emphasis is being placed on natural ingredients due to their bioavailability and absence of side effects. In regards to this claim, promising results have been witnessed in the usage of Ipomoea batatas (I. batatas) in treating the hyperglycemic and dyslipidemic condition. Thus, the aim of this paper is to conduct an overview of the reported effects of I. batatas focusing on in vitro and in vivo trials in reducing high glucose levels and regulating the dyslipidemic condition. A comprehensive literature search was performed using Scopus, Web of Science, Springer Nature, and PubMed databases to identify the potential articles on particular topics. The search query was accomplished based on the Boolean operators involving keywords such as (1) Beneficial effect OR healing OR intervention AND (2) sweet potato OR Ipomoea batatas OR traditional herb AND (3) blood glucose OR LDL OR lipid OR cholesterol OR dyslipidemia. Only articles published from 2011 onwards were selected for further analysis. This review includes the (1) method of intervention and the outcome (2) signaling mechanism involved (3) underlying mechanism of action, and the possible side effects observed based on the phytoconstiuents isolated. The comprehensive literature search retrieved a total of 2491 articles using the appropriate keywords. However, on the basis of the inclusion and exclusion criteria, only 23 articles were chosen for further review. The results from these articles indicate that I. batatas has proven to be effective in treating the hyperglycemic condition and is able to regulate dyslipidemia. Therefore, this systematic review summarizes the signaling mechanism, mechanism of action, and phytoconstituents responsible for those activities of I. batatas in treating hyperglycemic based on the in vitro and in vivo study.

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Sosa Alvarado C, Yang K, Qiu H, Mills E, Fouhse JM, Ju T, Buteau J, Field CJ, Willing BP, Chan CB. Transient antibiotic-induced changes in the neonatal swine intestinal microbiota impact islet expression profiles reducing subsequent function. Am J Physiol Regul Integr Comp Physiol 2021;321:R303-R316. [PMID: 34259034 DOI: 10.1152/ajpregu.00090.2021] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]

Abstract

Neonatal antibiotics administered to human infants initiate gut microbiota dysbiosis that may have long-term effects on body weight and metabolism. We examined antibiotic-induced adaptations in pancreatic islets of the piglet, a well-accepted model of human infant microbiota and pancreas development. Neonatal piglets randomized to amoxicillin [30 mg/kg body wt/day; n = 7, antibiotic (ANTI)] or placebo [vehicle control; n = 7, control (CON)] from postnatal day (PND)0-13 were euthanized at PND7, 14, and 49. The metabolic phenotype along with functional, immunohistological, and transcriptional phenotypes of the pancreatic islets were studied. The gut microbiome was characterized by 16S rRNA gene sequencing, and microbial metabolites and microbiome-sensitive host molecules were measured. Compared with CON, ANTI PND7 piglets had elevated transcripts of genes involved in glucagon-like peptide 1 ((GLP-1) synthesis or signaling in islets (P < 0.05) coinciding with higher plasma GLP-1 (P = 0.11), along with increased tumor necrosis factor α (Tnf) (P < 0.05) and protegrin 1 (Npg1) (P < 0.05). Antibiotic-induced relative increases in Escherichia, Coprococcus, Ruminococcus, Dehalobacterium, and Oscillospira of the ileal microbiome at PND7 normalized after antibiotic withdrawal. In ANTI islets at PND14, the expression of key regulators pancreatic and duodenal homeobox 1 (Pdx1), insulin-like growth factor-2 (Igf2), and transcription factor 7-like 2 (Tcf7l2) was downregulated, preceding a 40% reduction of β-cell area (P < 0.01) and islet insulin content at PND49 (P < 0.05). At PND49, a twofold elevated plasma insulin concentration (P = 0.07) was observed in ANTI compared with CON. We conclude that antibiotic treatment of neonatal piglets elicited gut microbial changes accompanied by phasic alterations in key regulatory genes in pancreatic islets at PND7 and 14. By PND49, reduced β-cell area and islet insulin content were accompanied by elevated nonfasted insulin despite normoglycemia, indicative of islet stress.

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Santoso CMA, Ketti F, Bramantoro T, Zsuga J, Nagy A. Association between Oral Hygiene and Metabolic Syndrome: A Systematic Review and Meta-Analysis. J Clin Med 2021;10:2873. [PMID: 34203460 PMCID: PMC8269064 DOI: 10.3390/jcm10132873] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/25/2021] [Revised: 06/14/2021] [Accepted: 06/18/2021] [Indexed: 12/14/2022] Open

Duan J, Song Y, Zhang X, Wang C. Effect of ω-3 Polyunsaturated Fatty Acids-Derived Bioactive Lipids on Metabolic Disorders. Front Physiol 2021;12:646491. [PMID: 34113260 PMCID: PMC8185290 DOI: 10.3389/fphys.2021.646491] [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] [Subscribe] [Scholar Register] [Received: 12/27/2020] [Accepted: 04/26/2021] [Indexed: 12/23/2022] Open

Al-Mofarji ST, Hussien H, Mohamed N, Hantoosh S, Abass M, Ali A. The association between gastric bacterial infection and low level of vitamin D among patients with type 2 diabetes mellitus. BAGHDAD JOURNAL OF BIOCHEMISTRY AND APPLIED BIOLOGICAL SCIENCES 2021. [DOI: 10.47419/bjbabs.v2i01.32] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022] Open

Mosavat M, Mirsanjari M, Arabiat D, Smyth A, Whitehead L. The Role of Sleep Curtailment on Leptin Levels in Obesity and Diabetes Mellitus. Obes Facts 2021;14:214-221. [PMID: 33756469 PMCID: PMC8138234 DOI: 10.1159/000514095] [Citation(s) in RCA: 24] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/30/2020] [Accepted: 12/23/2020] [Indexed: 12/15/2022] Open

Moreau M, Benhaddou S, Dard R, Tolu S, Hamzé R, Vialard F, Movassat J, Janel N. Metabolic Diseases and Down Syndrome: How Are They Linked Together? Biomedicines 2021;9:biomedicines9020221. [PMID: 33671490 PMCID: PMC7926648 DOI: 10.3390/biomedicines9020221] [Citation(s) in RCA: 26] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/16/2021] [Revised: 02/15/2021] [Accepted: 02/17/2021] [Indexed: 12/13/2022] Open

Coderre L, Debieche L, Plourde J, Rabasa-Lhoret R, Lesage S. The Potential Causes of Cystic Fibrosis-Related Diabetes. Front Endocrinol (Lausanne) 2021;12:702823. [PMID: 34394004 PMCID: PMC8361832 DOI: 10.3389/fendo.2021.702823] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/30/2021] [Accepted: 07/06/2021] [Indexed: 12/16/2022] Open

Expression of miRNA-29 in Pancreatic β Cells Promotes Inflammation and Diabetes via TRAF3. Cell Rep 2021;34:108576. [PMID: 33406428 DOI: 10.1016/j.celrep.2020.108576] [Citation(s) in RCA: 85] [Impact Index Per Article: 21.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/22/2020] [Revised: 10/23/2020] [Accepted: 12/09/2020] [Indexed: 12/18/2022] Open

Pakhomova A, Pershina O, Nebolsin V, Ermakova N, Krupin V, Sandrikina L, Pan E, Widera D, Dygai A, Skurikhin E. Bisamide Derivative of Dicarboxylic Acid Contributes to Restoration of Testicular Tissue Function and Influences Spermatogonial Stem Cells in Metabolic Disorders. Front Cell Dev Biol 2020;8:562358. [PMID: 33344442 PMCID: PMC7744787 DOI: 10.3389/fcell.2020.562358] [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: 05/15/2020] [Accepted: 09/30/2020] [Indexed: 11/13/2022] Open

Affiliation(s)

Angelina Pakhomova Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia
Olga Pershina Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia
Vladimir Nebolsin “PHARMENTERPRISES Ltd.,”Moscow, Russia
Natalia Ermakova Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia
Vyacheslav Krupin Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia
Lubov Sandrikina Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia
Edgar Pan Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia
Darius Widera Stem Cell Biology and Regenerative Medicine Group, School of Pharmacy, University of Reading, Reading, United Kingdom
Alexander Dygai Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia
Evgenii Skurikhin Laboratory of Regenerative Pharmacology, Goldberg ED Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Centre of the Russian Academy of Sciences, Tomsk, Russia

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Chen S, Sbuh N, Veedu RN. Antisense Oligonucleotides as Potential Therapeutics for Type 2 Diabetes. Nucleic Acid Ther 2020;31:39-57. [PMID: 33026966 DOI: 10.1089/nat.2020.0891] [Citation(s) in RCA: 16] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open

Carbone F, Bonaventura A, Liberale L, Paolino S, Torre F, Dallegri F, Montecucco F, Cutolo M. Atherosclerosis in Rheumatoid Arthritis: Promoters and Opponents. Clin Rev Allergy Immunol 2020;58:1-14. [PMID: 30259381 DOI: 10.1007/s12016-018-8714-z] [Citation(s) in RCA: 33] [Impact Index Per Article: 6.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]

Maluf S, Salgado JV, Cysne DN, Camelo DMF, Nascimento JR, Maluf BVT, Silva LDM, Belfort MRDC, Silva LA, Guerra RNM, Salgado Filho N, Nascimento FRF. Increased Glycated Hemoglobin Levels in Patients With Helicobacter pylori Infection Are Associated With the Grading of Chronic Gastritis. Front Immunol 2020;11:2121. [PMID: 33013895 PMCID: PMC7511518 DOI: 10.3389/fimmu.2020.02121] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/14/2020] [Accepted: 08/05/2020] [Indexed: 12/20/2022] Open

Abstract

Background

Recent studies have found an association between Helicobacter pylori infection and prediabetes. Whether H. pylori per se or host factors are involved in the disturbance of glycated hemoglobin needs further investigation. The aim of this study was to determine the association of glycated hemoglobin levels with endoscopic diagnosis and the inflammatory response in H. pylori infection.

Methods

A cross-sectional study was carried out in 88 dyspeptic non-diabetic adults who underwent esophagogastroduodenoscopy. The diagnosis of H. pylori infection was performed through urease test and histopathological exam. Cases were initially distributed into two groups: control (without H. pylori infection, n = 22) and HP (patients with H. pylori infection, n = 66). HbA1c was measured to determine prediabetes status according to the American Diabetes Association criteria, and then the groups were subdivided into non-prediabetic (n = 14), prediabetic (n = 8), non-prediabetic HP (n = 26) and prediabetic HP (n = 40) groups. Gastric mucosa was histologically evaluated to determine H. pylori density and inflammatory activity according to Sydney System. To investigate the balance of anti-inflammatory and pro-inflammatory cytokines we measured interleukin 10 (anti-inflammatory) and Tumor Necrosis Factor-a (pro-inflammatory) in the plasma or in the gastric mucosa.

Results

Patients with H. pylori infection had higher mean HbA1c levels than those without H. pylori infection. However, increased HbA1c levels were not associated with H. pylori-related factors but with the bacterial density, the intensity of inflammation and the activity of the chronic gastritis. In addition, H. pylori infection per se did not alter IL-10 and TNF-α neither in the plasma nor in the gastric mucosa, but the bacterial density was negatively correlated with systemic and local IL-10 expression. Although no correlation was found between systemic cytokines and HbA1c levels, local anti-inflammatory cytokine was correlated with HbA1c levels.

Conclusion

Long-term H. pylori infection is associated with prediabetes. This association is not related to the presence of H. pylori per se but depends on the extent of bacterial colonization and the degree of both local inflammation and activity of the chronic gastritis.

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Affiliation(s)

Selma Maluf Health Science Graduate Program, Federal University of Maranhão, São Luís, Brazil.,Gastroenterology Service of the University Hospital, Federal University of Maranhão, São Luís, Brazil.,Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil
João Victor Salgado Department of Physiological Sciences, Federal University of Maranhão, São Luís, Brazil
Dalila Nunes Cysne Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil
Daniel Monte Freire Camelo Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil
Johnny Ramos Nascimento Health Science Graduate Program, Federal University of Maranhão, São Luís, Brazil.,Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil
Bianca Vitória T Maluf Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil
Luís Douglas Miranda Silva Health Science Graduate Program, Federal University of Maranhão, São Luís, Brazil
Marta Regina de Castro Belfort Health Science Graduate Program, Federal University of Maranhão, São Luís, Brazil
Lucilene Amorim Silva Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil.,Department of Pathology, Federal University of Maranhão, São Luís, Brazil
Rosane Nassar Meireles Guerra Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil.,Department of Pathology, Federal University of Maranhão, São Luís, Brazil
Natalino Salgado Filho Department of Medicine I, Federal University of Maranhão, São Luís, Brazil
Flávia Raquel F Nascimento Immunophysiology Laboratory, Department of Pathology, Federal University of Maranhão, São Luís, Brazil.,Department of Pathology, Federal University of Maranhão, São Luís, Brazil

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Mussa BM, Srivastava A, Mohammed AK, Verberne AJM. Nitric oxide interacts with cholinoceptors to modulate insulin secretion by pancreatic β cells. Pflugers Arch 2020;472:1469-1480. [PMID: 32803305 PMCID: PMC7476970 DOI: 10.1007/s00424-020-02443-9] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/16/2020] [Revised: 07/17/2020] [Accepted: 07/31/2020] [Indexed: 01/09/2023]

Kouitcheu Mabeku LB, Noundjeu Ngamga ML, Leundji H. Helicobacter pylori infection, a risk factor for Type 2 diabetes mellitus: a hospital-based cross-sectional study among dyspeptic patients in Douala-Cameroon. Sci Rep 2020;10:12141. [PMID: 32699242 PMCID: PMC7376106 DOI: 10.1038/s41598-020-69208-3] [Citation(s) in RCA: 16] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/08/2020] [Accepted: 04/03/2020] [Indexed: 02/07/2023] Open

Abstract

Diabetic mellitus patients are usually prone to chronic infections. However, there have been contradictory reports about the association between H. pylori infection and type II diabetes. The present study is aimed at evaluating the prevalence of Helicobacter pylori infection among type 2 dyspeptic diabetic patients in the littoral region of Cameroon. This cross sectional study comprised 93 type 2 diabetic dyspeptic patients and 112 non-diabetic dyspeptic patients attending the Gastroenterology Department at two reference hospitals in Douala-Cameroon. The study was approved by the local Ethical Committee of Medical Sciences. Participants were screened for the presence of both type 2 diabetes and H. pylori infection. Body mass index (BMI) of all the participants was also recorded. Data was analyzed using SSPS statistical package. H. pylori infection was found in 73.11% of diabetic patients versus 58.05% in non-diabetic participants, this difference was found to be significant (OR = 1.472, p = 0.0279). This relationship persists even when adjusted to factors such as age and income level of participants. Infected participants from age group ≥ 55 years and those with high income were those with a higher risk to develop diabetes. Infected patients with high BMI were more prone to develops diabetic mellitus compared with infected patients with normal BMI (p = 0.0034). Also, participant with high BMI were more prone to develops diabetic mellitus whether they were infected or not. Patients having both H. pylori + ve and BMI ≥ 25 kg/m2 were significantly more affected by diabetic mellitus than those in the others combined groups (p < 0.0001), suggested that high BMI and H. pylori infection together or not are factors that favor diabetes mellitus development. Separately or not, H. pylori infection and high BMI were risk factor for diabetes mellitus in our milieu.

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Rattanaporn P, Tongsima S, Mandrup-Poulsen T, Svasti S, Tanyong D. Combination of ferric ammonium citrate with cytokines involved in apoptosis and insulin secretion of human pancreatic beta cells related to diabetes in thalassemia. PeerJ 2020;8:e9298. [PMID: 32587797 PMCID: PMC7304432 DOI: 10.7717/peerj.9298] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2020] [Accepted: 05/14/2020] [Indexed: 01/09/2023] Open

Truong NTT, Lydic TA, Bazil JN, Suryadevara A, Olson LK. Regulation of lipid metabolism in pancreatic beta cells by interferon gamma: A link to anti-viral function. Cytokine 2020;133:155147. [PMID: 32492632 DOI: 10.1016/j.cyto.2020.155147] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/13/2020] [Revised: 05/01/2020] [Accepted: 05/25/2020] [Indexed: 12/22/2022]

Antidiabetic Effects of Bisamide Derivative of Dicarboxylic Acid in Metabolic Disorders. Int J Mol Sci 2020;21:ijms21030991. [PMID: 32028560 PMCID: PMC7037053 DOI: 10.3390/ijms21030991] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/21/2020] [Revised: 01/31/2020] [Accepted: 01/31/2020] [Indexed: 01/02/2023] Open

Yang W, Chi Y, Meng Y, Chen Z, Xiang R, Yan H, Yang J. FAM3A plays crucial roles in controlling PDX1 and insulin expressions in pancreatic beta cells. FASEB J 2020;34:3915-3931. [PMID: 31944392 DOI: 10.1096/fj.201902368rr] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/16/2019] [Revised: 12/22/2019] [Accepted: 12/24/2019] [Indexed: 11/11/2022]

Narrow-Leafed Lupin (Lupinus angustifolius L.) Seeds Gamma-Conglutin is an Anti-Inflammatory Protein Promoting Insulin Resistance Improvement and Oxidative Stress Amelioration in PANC-1 Pancreatic Cell-Line. Antioxidants (Basel) 2019;9:antiox9010012. [PMID: 31877933 PMCID: PMC7023629 DOI: 10.3390/antiox9010012] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/03/2019] [Revised: 12/18/2019] [Accepted: 12/19/2019] [Indexed: 01/01/2023] Open

Hanchang W, Khamchan A, Wongmanee N, Seedadee C. Hesperidin ameliorates pancreatic β-cell dysfunction and apoptosis in streptozotocin-induced diabetic rat model. Life Sci 2019;235:116858. [DOI: 10.1016/j.lfs.2019.116858] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2019] [Revised: 08/29/2019] [Accepted: 09/07/2019] [Indexed: 12/12/2022]