Controversy remains as to which obesity measures better predict type 2 diabetes (T2D) risk in overweight or obese individuals. The objective of this study is to determine which commonly used obesity measures better reflect beta cell function and predict T2D risk in participants with overweight or obesity and to validate the findings using prospective cohort data.

Cross-sectional data from the Obesity Clinic of the Xiangya Hospital of the Central South University and prospective cohort from UK Biobank. BMI, waist circumference (WC), waist-to-hip ratio (WHpR), and waist-to-height ratio (WHtR) were measured. Primary outcomes included beta cell function indices in the cross-sectional study and the occurrence of diabetes obtained from UK Biobank data.

One thousand four hundred and ninety-seven participants with overweight or obesity (median age 29 years, 41% males) and 322,023 UK Biobank participants without diabetes at baseline (mean age 56.83 years, 50.4% males) were studied. WHpR had a stronger association with beta cell function and central body fat distribution than the other three obesity measures irrespective of glucometabolic states. WHpR associated positively with diabetes risk in participants using the hazard ratio scale (HR per SD increase of WHpR, 2.311, 95% CI 2.250-2.374).

WHpR is a superior index in reflecting central body obesity, estimating beta cell function, and predicting T2D risk in people with overweight or obesity compared to BMI, WC, and WHtR.

Obesity is a worldwide health crisis and poses significant challenges in critical care. Many studies suggest an 'obesity paradox', in which obesity, defined by body mass index (BMI), is associated with better outcomes. However, the inability of BMI to discriminate between fat and muscle or between visceral adipose tissue and subcutaneous adipose tissue, limits its prediction of metabolic ill health. We suggest that the 'obesity paradox' may be more reflective of the limitations of BMI than the protective effect of obesity. We explore the biological processes leading to visceral fat accumulation, and the evidence linking it to outcomes in critical illness. In the 'spillover' hypothesis of adipose tissue expansion, caloric excess and impaired expansion of storage capacity in the subcutaneous adipose tissue lead to accumulation of visceral adipose tissue. This is associated with a chronic inflammatory state, which is integral to the link between visceral adiposity, type 2 diabetes mellitus, and ischaemic heart disease. We review the current evidence on visceral adiposity and critical illness outcomes. In COVID-19, increased visceral adipose tissue, irrespective of BMI, is associated with more severe disease. This is mirrored in acute pancreatitis, suggesting visceral adiposity is linked to poorer outcomes in some hyperinflammatory conditions. We suggest that visceral adiposity's chronic inflammatory state may potentiate acute inflammation in conditions such as COVID-19 and acute pancreatitis. Further work is required to investigate other critical illnesses, especially sepsis and acute respiratory distress syndrome, in which current evidence is scarce. This may give further insights into pathophysiology and inform tailored treatment and nutrition strategies based on body fat distribution.

Little is known about the associations between changes in hepatic steatosis and changes in abdominal adiposity after metabolic bariatric surgery.

To evaluate the serial changes in hepatic steatosis and abdominal adiposity following sleeve gastrectomy (SG).

University hospital, Taiwan.

In this prospective study, patients who underwent SG and intraoperative liver biopsy were enrolled. Magnetic resonance imaging (MRI) was performed to assess the liver fat fraction (LFF), visceral adipose tissue (VAT) area, and subcutaneous adipose tissue (SAT) area. Liver fibrosis was assessed preoperatively via biopsy and the fibrosis-4 index (FIB-4) and postoperatively with the FIB-4.

Seventy-six metabolic dysfunction-associated steatotic liver disease (MASLD) patients, including 67 pure MASLD patients and 9 MASLD patients with combined etiologies, were enrolled. LFF and visceral-to-subcutaneous fat ratio were associated with metabolic dysfunction-associated steatohepatitis, and VAT area was associated with significant fibrosis (≥F2). Twelve months after SG, all MRI measurements significantly improved. The median LFF of pure MASLD patients decreased from 17.4% at baseline to 4.2% and 3.7% at the 6th and 12th postoperative months, respectively. Complete resolution of steatosis was achieved in 97.5% of patients at the 12th postoperative months. Using %VAT and %SAT reductions at the sixth postoperative month as references, LFF decreased more rapidly, with fold ratios of 1.3 and 1.8, respectively.

SG resulted in a significant decrease in hepatic steatosis and abdominal adiposity in patients with severe obesity, but hepatic steatosis improved faster than abdominal adiposity. Hepatic steatosis resolved in almost all patients 12 months after SG.

Adipose tissue is an immunologically active organ that controls host physiology, partly through the release of mediators termed adipokines. In obesity, adipocytes and infiltrating leukocytes produce adipokines, which include the hormones adiponectin and leptin and cytokines such as tumour necrosis factor and IL-1β. These adipokines orchestrate immune responses that are collectively referred to as metabolic inflammation. Consequently, metabolic inflammation characterizes metabolic disorders and promotes distinct disease aspects, such as insulin resistance, metabolic dysfunction-associated liver disease and cardiovascular complications. In this unifying concept, adipokines participate in the immunological cross-talk that occurs between metabolically active organs in metabolic diseases, highlighting the fundamental role of adipokines in obesity and their potential for therapeutic intervention. Here, we summarize how adipokines shape metabolic inflammation in mice and humans, focusing on their contribution to metabolic disorders in the setting of obesity and discussing their value as therapeutic targets.

The purpose of this systematic review and meta-analysis is to investigate the association of metabolic dysfunction-associated steatotic liver disease (MASLD) with arterial stiffness and enlighten on potential cardiometabolic co-factors.

A literature search in PubMed/Medline, Embase, Scopus, and Web of Science databases was conducted. All the observational studies comparing arterial stiffness indices between adults with Non-alcoholic Fatty Liver Disease (NAFLD), Metabolic Dysfunction Associated-Fatty Liver Disease (MAFLD), or MASLD and apparently healthy individuals with normal liver function were included. Pulse wave velocity (PWV) and augmentation index (AIx) were mainly used as arterial stiffness indices.

Fourty one unique studies were included in the systematic review, with 27 deemed eligible for meta-analysis. Patients with MASLD had increased carotid-femoral PWV (14 studies, Mean difference (MD): 0.96 m/s, 95% confidence interval (CI) 0.65-1.27, p < 0.001) compared with healthy individuals. This finding was independent from body mass index, triglycerides, high-density lipoprotein, systolic blood pressure, and fasting plasma glucose. Moreover, patients with MASLD had higher brachial-ankle PWV (13 studies, MD: 78.14 cm/s, 95% CI 60.37-95.90, p < 0.001) and AIx (7 studies, MD: 3.85%, 95% CI 0.87-6.82, p = 0.0195) compared with controls.

MASLD is correlated with increased arterial stiffness. This relation is unaffected by common cardiometabolic risk factors.

PROSPERO (ID: CRD42023468258).

The associations of waist circumference (WC), body mass index (BMI), lipid accumulation product (LAP), Chinese visceral adiposity index (CVAI), and triglyceride-glucose Index (TyG) with the risk of type 2 diabetes mellitus (T2DM) remained uncertain in Chinese middle-aged and elderly hypertensive patients.

A total of 1,965 hypertensive participants aged 45 years and elderly were included in the cross-sectional analysis, and 1,576 hypertensive participants without T2DM for the cohort analysis. In the cross-sectional study, binary logistic regression, restricted cubic splines (RCS), and receiver operating characteristic (ROC) were used to analyze the relationships between WC, BMI, LAP, CVAI, and TyG with and T2DM in hypertensive patients. In the cohort study, Kaplan-Meier survival analyses and Cox regression were further performed to determine the associations of these indicators with incident T2DM risk.

In the cohort study, there were 101 incident T2DM cases occurred during a median follow-up of 30 months, with an incident rate was 2.78 per 100 person-years. The cross-sectional study showed that the risk of T2DM increased significantly with higher quartiles of WC, BMI, LAP, CVAI, and TyG (all P -trend < 0.001). In the cohort study, Cox regression model showed that WC (Q4 vs. Q1, HR = 3.30, 95% CI = 1.66-6.59), BMI (Q4 vs. Q1, HR = 2.38, 95% CI = 1.30-4.36), LAP (Q4 vs. Q1, HR = 5.15, 95% CI = 2.40-11.02), CVAI (Q4 vs. Q1, HR = 3.38, 95% CI = 1.76-6.50), and TyG (Q4 vs. Q1, HR = 5.76, 95% CI = 2.82-11.77) were associated with a higher risk of incident T2DM. RCS confirmed the positive dose-response relationships of WC, BMI, CVAI and TyG with T2DM in both study design, except for LAP in the cohort study. Additionally, ROC analysis revealed that TyG had the strongest area under the curve (AUC) of 0.70 (95% CI = 0.67-0.72) in the cross-sectional study, and the AUC of other indicators ranged from 0.55 to 0.57.

Higher levels of WC, BMI, LAP, CVAI, and TyG are associated with a higher riskof developing incident T2DM in Chinese elderly hypertensive patients, and TyG might be the most effective predictive indicator.

To elucidate risk factors associated with adverse perinatal outcomes in early-gestational diabetes mellitus (GDM).

A dataset of 385 early-GDM cases from a prospective cohort was analyzed. Early-GDM was diagnosed if one or more of the following criteria were met: fasting plasma glucose (PG) levels of 92-125 mg/dL, 1-h PG levels ≥180 mg/dL, and 2-h PG levels ≥153 mg/dL during a 75-g oral glucose tolerance test before 20 weeks of gestation. Multivariate analysis was used to examine associations between candidate risk factors and a composite outcome of maternal and neonatal adverse events.

Pre-pregnancy overweight/obesity (pre-pregnancy body mass index [BMI] ≥25.0 kg/m2) was significantly associated with a higher risk of the composite outcome compared with normal weight (pre-pregnancy BMI of 18.5-24.9 kg/m2), an adjusted risk ratio (aRR) of 1.44 (95% confidence interval [CI]: 1.08-1.93), and an adjusted risk difference (aRD) of 13.6% (95% CI: 2.6-24.6%). Compared with fasting PG levels below 92 mg/dL, levels between 95 and 125 mg/dL were associated with a significantly higher risk of the composite outcome, with an aRR and aRD of 1.42 (95% CI: 1.01-1.99) and 12.9% (95% CI: 0.3-25.5%), respectively.

Early-GDM, combined with pre-pregnancy overweight/obesity and/or fasting PG levels of 95-125 mg/dL, is associated with a higher risk of adverse perinatal outcomes and should be prioritized for intervention.

The visceral adiposity index is a valuable tool for assessing visceral fat accumulation. However, its non-linear association with prediabetes and diabetes requires further elucidation. Therefore, we aim to clarify the intricate interplay between the visceral adiposity index and these dysglycemic conditions.

The National Health and Nutrition Examination Survey database from 1999 to 2018 was utilized to analyze health data from 24,072 participants. A multivariate logistic regression model was employed to evaluate the independent association between the visceral adiposity index and prediabetes and diabetes while considering potential confounding factors. Generalized additive models were used to identify any non-linear relationships by fitting smooth curves. Additionally, a stratified analysis based on different baseline characteristics was conducted, along with an interactive analysis.

After accounting for all relevant variables, individuals in the lowest quartile of the visceral adiposity index had a notably diminished likelihood of progressing to prediabetes and diabetes when compared with those in the other three quartiles. The odds ratios and 95% confidence intervals were as follows: 1.37 (1.23, 1.53), 1.87 (1.65, 2.12), and 2.80 (2.33, 3.37). More importantly, a non-linear association was observed between the visceral adiposity index and prediabetes and diabetes, with a threshold identified at 2.10.

There exists a notable and positive association between the visceral adiposity index and prediabetes and diabetes, displaying non-linear attributes in this evaluation of the relationship. Risk assessment and early prevention strategies targeting the maintenance of low levels of visceral adiposity index may substantially diminish the likelihood of developing prediabetes and diabetes.

The present work focused on investigating the relation of visceral fat metabolic score (METS-VF) with cataract prevalence among the American adults.

A cross-sectional study.

This cross-sectional study, based on the U.S. population, used data from the National Health and Nutrition Examination Survey (NHANES) conducted between 1999 and 2008. For assessing the association of METS-VF with cataract, we employed multivariable logistic regression analysis, subgroup analyses, and restricted cubic splines (RCS) analysis for exploring their relation. Additionally, receiver operating characteristic (ROC) curve analysis was conducted to compare the cataract diagnostic abilities of METS-VF, body mass index (BMI), waist circumference (WC), and waist-to-height ratio (WHtR).

There were altogether 2,730 participants included, of whom 290 had cataract.METS-VF was significantly related to cataract (P < .001). As METS-VF quartiles increased, cataract prevalence also increased (Q1: 1.90%, Q2: 6.74%, Q3: 10.25%, Q4: 23.61%). After adjusting for all variables, METS-VF still showed positive relation to cataract prevalence (odds ratio (OR) = 3.14, 95% confidence interval (CI): 1.67, 5.93). Subgroup analysis revealed a consistent relationship between METS-VF and cataracts across different groups. The RCS results showed that there was no significant nonlinear relationship between METS-VF and cataracts (P-non-linear = 0.209). ROC curve analysis showed that METS-VF outperformed BMI, WC, and WHtR in cataract prediction.

METS-VF is significantly positively related to a higher cataract prevalence, and this relationship remains robust across various subgroups. Additionally, METS-VF demonstrates a stronger predictive ability for cataract than BMI, WC, and WHtR.

Insulin and iron availability stimulate and regulate erythropoiesis, respectively. The effects of hyperinsulinemia and/or iron overload on erythroid differentiation are unclear.

Male C57Bl/6J wild-type (WT) mice were fed a high-fat diet (HFD) (to produce hyperinsulinemia) or a control diet (CD) for varying periods (4-24 weeks). Hepcidin knock-out (Hamp1 -/- ) mice (which are iron-overloaded) were fed CD or HFD for 24 weeks. Terminal erythroid differentiation (TED) in the bone marrow (BM) from these mice was analyzed by flow cytometry. Hematological parameters were estimated in peripheral blood.

HFD-feeding of WT mice did not significantly affect erythroid precursors in the BM or hematological parameters. However, these mice had a significantly higher reticulocyte population in the BM than those fed CD (at all time points studied). Values of hematological parameters were higher in Hamp1 -/- mice than WT mice, at 24 weeks of feeding (irrespective of diet type), indicating increased erythropoiesis. Early erythroid precursors in the BM were higher in HFD-fed Hamp1 -/- mice than those fed CD.

HFD-feeding in WT mice resulted in increases in the proportion of reticulocytes in the bone marrow; maturation of the early erythroid precursors was not significantly affected. In Hamp1 -/- mice, HFD-feeding increased the number of early erythroid precursors.

We aimed to explore the predictive significance of the nutritional indexes in the occurrence of postoperative leakage after gastrectomy, aiming to develop and validate a predictive nomogram for assessing the risk of these complications.

Patients undergoing radical gastrectomy for gastric cancer were studied, using data from The Sixth Affiliated Hospital of Sun Yat-sen University (2019-2022, n = 1075) for nomogram development and an external cohort from Sun Yat-sen University Cancer Center (2022, n = 286) for validation. The model, focusing on postoperative leakage, was constructed through univariate and backward stepwise regression. The performance of nomogram was assessed using the receiver operating characteristic (ROC) curve, calibration plots, decision curve analysis (DCA), and clinical impact curves (CIC).

The incidence rates of postoperative leakage were 6.51% in the training cohort and 6.71% in the external validation cohort, respectively. The nomogram effectively identifies critical factors influencing postoperative leakage risk, including NRS-2002 score, SFMAI, VSR, blood loss, intraoperative time, type of reconstruction, and Lauren type. The areas under the curve (AUC) for the development and external validation cohorts were 0.763 and 0.761, respectively, demonstrating acceptable predictive accuracy. The validation study showed the nomogram's satisfactory calibration, and both DCA and CIC confirmed its significant clinical utility.

The nomogram offers an efficient and precise tool for initial screening, effectively identifying individuals at elevated risk for postoperative leakage.

Extracellular vesicles (EVs) represent a sophisticated mechanism of intercellular communication that is implicated in health and disease. Specifically, the role of EVs in metabolic regulation and their implications in metabolic pathologies, such as obesity and its comorbidities, remain unclear.

Extracellular vesicles (EVs) were isolated through serial ultracentrifugation from murine adipocytes treated with palmitate or oleic acid, whole visceral and subcutaneous adipose tissue (obesesomes) of bariatric surgery obese donors, and human hepatocytes under steatosis (steatosomes) for functional in vitro experiments. Functional effects on inflammation and glucose and lipid metabolism of target cells (human and murine macrophages and hepatocytes) were assessed using ELISA, RT-PCR, and immunodetection. Isolated EVs from human steatotic (steatosomes) and control hepatocytes (hepatosomes) were characterized for quantity, size, and tetraspanin profile by NTA and Single Particle Interferometric Reflectance Imaging Sensor (SP-IRIS), and their protein cargo analyzed by qualitative (DDA) and quantitative (DIA-SWATH) proteomics using LC-MS/MS. Proteins identified by proteomics were validated by capturing EVs on functionalized chips by SP-IRIS.

In this study, we investigated the role of EVs in the local communication between obese adipocytes and immune cells within adipose tissue, and the interaction of steatotic and healthy hepatocytes in the context of fatty liver disease progression. Furthermore, we analyzed obese adipose tissue-to-liver interactions through EV-obesesomes to elucidate their role in obesity-associated hepatic metabolic dysregulation. Our findings reveal that obesesomes promote inflammation and the secretion of pro-inflammatory cytokines upon interaction with macrophages, exerting a significant impact on reducing insulin resistance and altering lipid and glucose metabolism upon interaction with hepatocytes; in both cases, EVs from palmitate-loaded adipocytes and obesesomes from human visceral adipose depots demonstrated the most deleterious effect. Additionally, EVs secreted by steatotic hepatocytes (steatosomes) induced insulin resistance and altered lipid and glucose metabolism in healthy hepatocytes, suggesting their involvement in MASLD development. Proteomic analysis of steatosomes revealed that these vesicles contain liver disease-associated proteins, rendering them significant repositories of real-time biomarkers for the early stages and progression of MASLD.

Obesity is an independent risk factor for increased disease severity during influenza A virus (IAV) infection. White adipose tissue (WAT) inflammation promotes disease pathogenesis in obesity. Whether obesity modifies lung and WAT immune cells to amplify influenza severity is unknown. We show that obesity establishes a proinflammatory transcriptome in lung immune cells that is augmented during IAV infection and that IAV infection changes WAT immune cell milieu in obesity. Notably, a decrease in WAT macrophages (ATM) inversely correlates with an increase in infiltrating lung macrophages in obese IAV-infected mice. Further analyses of lung immune cell uncovered a macrophage subset that shares a transcriptomic signature with inflammatory ATMs. Importantly, adoptive transfer of ATMs from obese mice into lean IAV infected mice promotes host immune cell infiltration to the lungs. These findings suggest that, in an obese state, ATMs may exacerbate the inflammatory milieu important in pathologic responses to IAV infection.

To assess the associations between the creatinine-to-body weight (Cre/BW) ratio and reversion to normoglycemia mediated by the aspartate aminotransferase-to-alanine aminotransferase (De Ritis) ratio. This retrospective cohort study included 24,884 prediabetic participants from health check-ups in 32 regions across 11 Chinese cities. We employed multivariable Cox regression to assess time-to-event outcomes, smooth curve fitting for trend analysis, and inflection point analysis to determine critical thresholds. Subgroup analyses were performed to explore interactions. Mediation analysis was conducted to clarify the mechanisms linking prediabetes with health outcomes. In the analysis of 24,884 individuals, it was observed that 49.08% of the prediabetic subjects experienced normoglycemic conversion during a follow-up period spanning 73,517.66 person-years. Following full adjustment, the Cre/BW ratio was positively associated with normoglycemic conversion among prediabetic individuals (HR 1.42, 95% CI 1.30-1.55). Multivariate smooth spline analysis revealed a nonlinear relationship between the Cre/BW ratio and glucose status conversion (P for nonlinearity < 0.05), with the curves leveling off when the Cre/BW ratio (×100) reached 1.34. Subgroup analysis and additional sensitivity analyses confirmed that the results between the Cre/BW ratio and glucose status conversion were robust. Additionally, the De Ritis ratio was found to explain 50% of the association between the Cre/BW ratio and the prediabetes-to-normoglycemia transition. A higher Cre/BW ratio was associated with a better chance of controlling blood glucose levels in prediabetic individuals, with the De Ritis ratio playing a key mediating role.

The intricate relationship between systemic immune-inflammation index (SII) and trimethylamine N-oxide (TMAO) in the peripheral blood and osteoporosis (OP) remains unclear. This study aims to investigate variations in the levels of SII and TMAO in the peripheral blood of overweight and obese patients, and examine the associations between these markers, bone mineral density (BMD), and the occurrence of osteoporotic fractures.

The study enrolled 765 patients aged ≥ 50 years with BMI ≥ 24 kg/m², dividing them into two groups based on visceral fat area (VFA): <100 cm² and ≥100 cm². A corrected regression model analyzed the association of SII, TMAO, BMD, and osteoporotic fractures incidence in patients with central obesity. Receiver operator characteristic (ROC) curves assessed the predictive ability of SII and TMAO for OP screening.

Baseline data showed that patients with VFA ≥ 100 cm² had lower whole body (WB) and lumbar spine (LS) BMD, but higher SII and TMAO levels compared to those with VFA < 100 cm² (p < 0.05). Particularly in the group with VFA ≥ 100 cm2, there was an upward trend in SII and TMAO as bone mass decreased. Regression analysis found SII and TMAO negatively correlated with WB, LS, and femoral neck (FN) BMD, and positively correlated with osteoporotic fractures incidence (p < 0.05). Both were independent risk factors for OP, with combined SII and TMAO detection showing high diagnostic efficacy (sensitivity 94.7%, specificity 96.5%).

In overweight and obese patients, particularly those with a VFA ≥ 100 cm², peripheral blood SII and TMAO levels may serve as valuable biomarkers for the early diagnosis of OP, offering potential clinical utility in identifying high-risk individuals.

The 'Body Mass Index' (BMI) is an anachronistic and outdated ratio that is used as an internationally accepted diagnostic criterion for obesity, and to prioritise, stratify, and outcome-assess its management options. On an individual level, the BMI has the potential to mislead, including inaccuracies in cardiovascular risk assessment. Furthermore, the BMI places excessive emphasis on a reduction in overall body weight (rather than optimised body composition) and contributes towards a misunderstanding of the quiddity of obesity and a dispassionate societal perspective and response to the global obesity problem. The overall objective of this review is to provide an overview of obesity that transitions away from the BMI and towards a novel vista: viewing obesity from the perspective of the skeletal muscle (SM). We resurrect the SM as a tissue hidden in plain sight and provide an overview of the key role that the SM plays in influencing metabolic health and efficiency. We discuss the complex interlinks between the SM and the adipose tissue (AT) through key myokines and adipokines, and argue that rather than two separate tissues, the SM and AT should be considered as a single entity: the 'Adipo-Muscle Axis'. We discuss the vicious circle of sarcopenic obesity, in which aging- and obesity-related decline in SM mass contributes to a worsened metabolic status and insulin resistance, which in turn further compounds SM mass and function. We provide an overview of the approaches that can mitigate against the decline in SM mass in the context of negative energy balance, including the optimisation of dietary protein intake and resistance physical exercises, and of novel molecules in development that target the SM, which will play an important role in the future management of obesity. Finally, we argue that the Adipo-Muscle Ratio (AMR) would provide a more clinically meaningful descriptor and definition of obesity than the BMI and would help to shift our focus regarding its effective management away from merely inducing weight loss and towards optimising the AMR with proper attention to the maintenance and augmentation of SM mass and function.

While the connection between the Triglyceride glucose-waist circumference (TyG-WC) index and the risk of diabetes remains understudied, this particular research delves into the potential predictive value of the TyG-WC index within a significant Japanese population.

This retrospective cohort study encompassed a comprehensive analysis of 15,413 Japanese adults, all of whom were diabetes-free at the outset of the study period from 2004 to 2015. Comprehensive medical records were obtained for all participants who underwent physical examinations. The study employed Cox proportional-hazards regression, smooth curve fitting, various sensitivity, and subgroup analyses to explore the association between TyG-WC and the development of diabetes. Furthermore, a Receiver Operating Characteristic (ROC) curve was created to detect the predictive capability of TyG-WC for diabetes risk.

After a maximum of 13.0 years of follow-up, 358 people finally developed diabetes. Upon adjusting for covariates, the result showed TyG-WC was positively and independently associated with incident Diabetes Mellitus (DM) (Hazard Ratio (HR): 1.004, 95%C: 1.001-1.006). Furthermore, ROC curve analysis demonstrated that TyG-WC outperformed both the triglycerides-glucose index and triglyceride glucose-body mass index in predicting the onset of diabetes.

High levels of TyG-WC are autonomously linked to a heightened risk of diabetes in the Japanese demographic, indicating its potential as a dependable predictive indicator for diabetes mellitus in individuals at elevated risk.

Multifaceted factors play a crucial role in the prevention and treatment of metabolic dysfunction-associated steatotic liver disease (MASLD). This study aimed to utilize multifaceted indicators to construct MASLD risk prediction machine learning models and explore the core factors within these models.

MASLD risk prediction models were constructed based on seven machine learning algorithms using all variables, insulin-related variables, demographic characteristics variables, and other indicators, respectively. Subsequently, the partial dependence plot(PDP) method and SHapley Additive exPlanations (SHAP) were utilized to explain the roles of important variables in the model to filter out the optimal indicators for constructing the MASLD risk model.

Ranking the feature importance of the Random Forest (RF) model and eXtreme Gradient Boosting (XGBoost) model constructed using all variables found that both homeostasis model assessment of insulin resistance (HOMA-IR) and triglyceride glucose-waist circumference (TyG-WC) were the first and second most important variables. The MASLD risk prediction model constructed using the variables with top 10 importance was superior to the previous model. The PDP and SHAP methods were further utilized to screen the best indicators (including HOMA-IR, TyG-WC, age, aspartate aminotransferase (AST), and ethnicity) for constructing the model, and the mean area under the curve value of the models was 0.960.

HOMA-IR and TyG-WC are core factors in predicting MASLD risk. Ultimately, our study constructed the optimal MASLD risk prediction model using HOMA-IR, TyG-WC, age, AST, and ethnicity.

Olive cake was incorporated at a low inclusion rate (3.7%) into the rations of dairy cows through partial substitution of maize, and its effects on milk production, general health, and fertility traits were investigated. Multiparous purebred Holstein dairy cows (n = 148) were divided into two groups: a treated group (n = 86) and a control group (n = 62). The control ration (group C) was modified by replacing 1 kg of maize with an equal quantity of olive cake (group T). The experiment lasted from 60 days prepartum to 150 days postpartum. Electronic aids were utilized to quantify daily milk yield and detect estrus expression, while clinical and uterine examinations were performed weekly. Blood samples, uterine epithelial cells, and endometrial tissue samples were collected from a subgroup of healthy animals in both groups at specific time points. Blood samples were examined to determine the β-hydroxybutyric acid (BHBA), acute phase proteins (haptoglobin [Hpt] and serum amyloid A [SAA]), progesterone, and pregnancy-associated glycoproteins concentrations. Uterine epithelial cells were assessed for polymorphonuclear neutrophil (PMN) counts, and the expression of nine genes encoding inflammatory cytokines and immune system activation was analyzed in uterine biopsy tissue. No significant differences (p > 0.05) were observed between groups in milk yield, general morbidity, clinical endometritis, or conception rates. However, animals in group T came to estrus approximately 6 days earlier (p = 0.013) than those in group C; progesterone concentrations on day 7 of the subsequent cycle tended (p = 0.07) to be higher in group T. On day 21, BHBA concentrations were higher in group C than in group T (p < 0.05). Throughout the experiment, Hpt levels in group T were consistently lower (p < 0.001), while SAA was lower on day 7 compared to group C. From days 21 to 42 postpartum, there was a significant reduction in PMN numbers (group C p = 0.02; group T p < 0.0001), with a tendency for a greater reduction rate in group T (p = 0.08). Among the genes studied, a significant difference was revealed in the expression of the ILA1 gene, with strong correlations of gene expression in group C and weak to moderate correlations in group T. In conclusion, under the conditions of this experiment, the inclusion of olive cake into dairy cows' rations did not affect milk production but improved certain health and fertility parameters, making olive cake a suitable alternative feedstuff for high-producing animals.

Cardiometabolic index (CMI), visceral adiposity index (VAI), and lipid accumulation product (LAP) are lipid-related parameters that reflect central obesity, which is closely associated with the development of non-alcoholic fatty liver disease (NAFLD). The aim of this study is to investigate the effectiveness of these lipid-related parameters in diagnosing NAFLD and to compare their predictive abilities.

This population-based study extracted datasets from the National Health and Nutrition Examination Survey (NHANES) 2017-2020. CMI, VAI, and LAP were included in the multivariate logistic model as both continuous and categorical variables to assess the relationship between different lipid-related parameters and NAFLD. To further elucidate this connection, we utilized restricted cubic splines and conducted subgroup analysis. Additionally, the receiver operating characteristics (ROC) curve was employed to evaluate the predictive effectiveness of CMI, VAI, and LAP for NAFLD.

The study included 2,878 adults as the study population, of whom 1,263 participants were diagnosed with NAFLD. When lipid-related parameters were analyzed as continuous variables, they showed a positive correlation with NAFLD. The OR(95%CI) were 2.29(1.81,2.89) for CMI (per 1-unit), 1.40(1.28,1.52) for VAI (per 1-unit) and 1.15(1.11,1.20) for LAP (per 10-units). This correlation remains statistically significant when the lipid-related parameters are analyzed as categorical variables. In descending order of diagnostic capability for NAFLD, the AUC values are as follows: LAP (0.794), CMI (0.752), and VAI (0.719).

CMI, VAI, and LAP may be important clinical indicators for identifying NAFLD, with LAP demonstrating the best predictive ability among them.

This study investigated how obesity, BMI ≥ 30 kg/m2, abdominal adiposity, and systemic inflammation relate to neuroinflammation using diffusion basis spectrum imaging.

We analyzed data from 98 cognitively normal midlife participants (mean age: 49.4 [SD 6.2] years; 34 males [34.7%]; 56 with obesity [57.1%]). Participants underwent brain and abdominal magnetic resonance imaging (MRI), blood tests, and amyloid positron emission tomography (PET) imaging. Abdominal visceral and subcutaneous adipose tissue (VAT and SAT, respectively) was segmented, and Centiloids were calculated. Diffusion basis spectrum imaging parameter maps were created using an in-house script, and tract-based spatial statistics assessed white matter differences in high versus low BMI values, VAT, SAT, insulin resistance, systemic inflammation, and Centiloids, with age and sex as covariates.

Obesity, high VAT, and high SAT were linked to lower axial diffusivity, reduced fiber fraction, and increased restricted fraction in white matter. Obesity was additionally associated with higher hindered fraction and lower fractional anisotropy. Also, individuals with high C-reactive protein showed lower axial diffusivity. Higher restricted fraction correlated with continuous BMI and SAT particularly in male individuals, whereas VAT effects were similar in male and female individuals.

The findings suggest that, at midlife, obesity and abdominal fat are associated with reduced brain axonal density and increased inflammation, with visceral fat playing a significant role in both sexes.

Individuals with metabolic syndrome have a high risk of developing cardiovascular disorders that is closely tied to visceral adipose tissue dysfunction, as well as an altered interaction between adipose tissue and the cardiovascular system. In metabolic syndrome, adipose tissue dysfunction is associated with increased hypertrophy, reduced vascularization, and hypoxia of adipocytes, leading to a pro-oxidative and pro-inflammatory environment. Among the pathways regulating adipose tissue homeostasis is the wingless-type mammary tumor virus integration site family (Wnt) signaling pathway, with both its canonical and non-canonical arms. Various modulators of the Wnt signaling have been identified to contribute to the development of metabolic diseases and their cardiovascular complications, with a particularly significant role played by Glycogen Synthase Kinase-3β (GSK-3β). GSK-3β levels and activities have various and often contrasting roles in obesity and related metabolic disorders, as well as their cardiovascular sequelae. Here, we explore the possibility that altered Wnt signaling and GSK-3β activities could serve as a connection between adipose tissue dysfunction and the development of cardiovascular disease in individuals with metabolic syndrome. We attempt to define a context-specific approach for intervention, which could possibly serve as a novel disease modifying therapy for the mitigation of such complications.

Approximately 3.5% of pregnancies in the United Kingdom are complicated by gestational diabetes mellitus (GDM). Risk factors for this mirror those contributing to type 2 diabetes (T2DM). Though socioeconomic status (SES) is presumed to contribute to GDM, evidence in the United Kingdom is limited. In this unique study, we explored the impact of SES on GDM prevalence in a London suburb population.

Four thousand one hundred and sixty-three pregnant women who booked between July 2018 and March 2020 at Princess Royal University Hospital were retrospectively analyzed. Associations between GDM prevalence and SES trends (using multiple deprivation deciles (MDD)), and body mass index (BMI), age, ethnicity, screening uptake, birth-weights and birth outcomes, were analyzed.

Patients with BMI >30 kg/m2, older than 35 years, and non-Caucasian ethnicity have an increased risk of developing GDM (p < 0.0001, p < 0.0001, p < 0.0001, respectively). No association existed between MDD and GDM prevalence (p-values over 0.05). Patients with risk factors for GDM were highest in the deprived areas p < 0.0001. MDD 1-4 (most deprived) had the highest percentage of missed screening (15% of patients with risk factors missed screening), compared to 8% in the least deprived group (p < 0.0001).

Our data surprisingly suggest that low SES did not increase the incidence of GDM, despite a higher proportion of women with risk factors for GDM living in the most deprived postcodes. However this unclear finding may be due to low screening uptake of deprived populations, and therefore lack of GDM diagnosis, or indicate that GDM is a result of a different aetiology to T2DM. Further research is needed to explore if access to screening services, lack of health education or other health inequalities were responsible for the high proportion of missed screening opportunities in deprived areas.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and its severe subgroup metabolic dysfunction-associated steatohepatitis (MASH) have become a global epidemic and are driven by chronic overnutrition and multiple genetic susceptibility factors. The physiological outcomes include hepatocyte death, liver inflammation and cirrhosis. The first therapeutic for MASLD and MASH, resmetirom, has recently been approved for clinical use and has energized this therapeutic space. However, there is still much to learn in clinical studies of MASH, such as the scale of placebo responses, optimal trial end points, the time required for fibrosis reversal and side effect profiles. This Review introduces aspects of disease pathogenesis related to drug development and discusses two main therapeutic approaches. Thyroid hormone receptor-β agonists, such as resmetirom, as well as fatty acid synthase inhibitors, target the liver and enable it to function within a toxic metabolic environment. In parallel, incretin analogues such as semaglutide improve metabolism, allowing the liver to self-regulate and reversing many aspects of MASH. We also discuss how combinations of therapeutics could potentially be used to treat patients.

Obesity is a significant part of the factors affecting lung function, and the assessment of obesity using the Metabolic Score for Visceral Fat (METS-VF) is more precise than other indicators like waist circumference and body mass index. This study investigated the relationship between lung function and METS-VF in The National Health and Nutrition Examination Survey (NHANES) database from 2007 to 2012.

The data utilized in this study was obtained from National Health and Nutrition Examination Survey spanning the years 2007 to 2012. A multivariate linear regression analysis was employed to investigate the association between METS-VF and lung function, followed by subgroup analysis to identify populations that may exhibit heightened sensitivity. Nonlinear correlations were assessed by fitting a restricted cubic spline, with validation of results conducted via threshold effect analysis.

In a study involving 4,356 participants, a weighted multiple linear regression model revealed a significant negative association between the METS-VF and forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), FEV1/FVC ratio, and forced expiratory flow between 25 and 75% of FVC (FEF25-75%). However, no association was observed with peak expiratory flow rate (PEF). When dividing the METS-VF into thirds, participants in the highest third exhibited significantly decreased levels of FEV1 (β: -342, 95%CI: -440, -245, p < 0.001), FVC (β: -312, 95%CI: -431, -192, p < 0.001), FEV1/FVC (β: -0.020, 95%CI: -0.030, -0.010, p < 0.001), and FEF25-75% (β: -424, 95%CI: -562, -285, p < 0.001). However, there was no significant relationship with PEF (β: -89, 95%CI: -325, 147, p = 0.446). RCS curve indicated a nonlinear negative correlation between METS-VF and FEV1, FVC, and FEV1/FVC. For FEV1, a significant negative correlation was found when the METS-VF < 6.426 (β = -158.595, 95%CI: -228.183, -89.007). This negative association became more pronounced when the METS-VF > 6.426 (β = -314.548, 95%CI: -387.326, -241.770). For FVC, a negative association was observed when the METS-VF < 6.401, (β = -5.477, 95%CI: -91.655, 80.702), but it did not reach statistical significance. However, METS-VF > 6.401, METS VF and lung function show a significant negative correlation (β = -399.288, 95%CI: -486.187, -312.388). FEV1/FVC showed a negative correlation only before the inflection point (METS-VF < 6.263) (β = -0.040, 95%CI: -0.047, -0.032), after the inflection point (METS-VF > 6.263), no correlation was found, but there was no statistical significance (β = 0.000; 95%CI: -0.006, 0.007), and METS-VF had a linear negative correlation with FEF25-75%. Subgroup analysis showed that the association was consistent across a variety of demographic factors, including age, sex, race, hypertension, and coronary heart disease. In addition, we found a stronger association between men under 40 and lung function.

METS-VF showed a linear negative correlation with FEF25-75%, and a nonlinear negative correlation with FEV1, FVC, FEV1/FVC, and FEF25-75%, but was not associated with PEF, particularly among males under the age of 40. These findings offer valuable insights into managing lung function by controlling visceral fat.

Systemic inflammation is reported in normal-weight obesity (NWO) and metabolically healthy obesity (MHO), which may be linked to their increased cardiovascular disease (CVD) risk. Yet, drivers of this inflammation remain unclear. We characterized factors known to influence inflammatory status (i.e., intestinal permeability, adipose tissue, diet quality, microbiota), and their relationships with measured inflammation, in NWO and MHO, healthy control subjects (CON), and metabolically unhealthy obesity (MUO; N = 80; n = 20/group). Serum indicators of intestinal permeability and inflammation were assessed by ELISA and/or multiplex. Total, visceral, and percent body fat were measured with dual-energy X-ray absorptiometry (DXA). Fecal microbiota composition was assessed via 16S rRNA sequencing (n = 9-10/group). For C-reactive protein (CRP), MUO > NWO > CON (P < 0.0001). In MHO, CRP was intermediate and similar to both MUO and NWO. Lipopolysaccharide binding protein (LBP) and the ratio of LBP to soluble CD14 (sCD14) were higher in MHO and MUO vs. CON/NWO (P < 0.0001). Across correlation and regression analyses, LBP consistently displayed the strongest relationships with CRP in the entire sample (r = 0.78; β = 0.57; P < 0.0001) and in MHO (r = 0.74; P < 0.01) but not NWO (r = 0.37; P = 0.11). Shannon index was higher in CON compared with MUO (P < 0.05) and inversely correlated with CRP in the full sample (r = -0.37; P < 0.05). These data are consistent with the notion that intestinal permeability is associated with low-grade inflammation in MHO, which could be implicated in this population's reported CVD risk.NEW & NOTEWORTHY This is the first study to our knowledge to examine biomarkers of intestinal permeability in normal-weight obesity and one of few assessing microbiota compositions in this population. Additionally, we report that individuals with metabolically healthy obesity and metabolically unhealthy obesity displayed similar evidence of intestinal permeability, which was more strongly associated with systemic inflammation than total and visceral adipose tissue mass.

Understanding of the pathophysiology of heart failure with preserved ejection fraction (HFpEF) has advanced rapidly over the past two decades. Currently, HFpEF is recognized as a heterogeneous syndrome, and there is a growing movement towards developing personalized treatments based on phenotype-guided strategies. Left ventricular dysfunction is a fundamental pathophysiological abnormality in HFpEF; however, recent evidence also highlights significant roles for the atria, right ventricle, pericardium, and extracardiac contributors. Imaging plays a central role in characterizing these complex and highly integrated domains of pathophysiology. This review focuses on established evidence, recent insights, and the challenges that need to be addressed concerning the pathophysiology of HFpEF, with a focus on imaging-based evaluations and opportunities for further research.

This study aimed to investigate the correlation between computed tomography (CT) derived body composition and 30-day mortality in patients with pulmonary infections caused by carbapenem-resistant Klebsiella pneumoniae (K. pneumoniae).

A total of 89 eligible participants from a tertiary teaching hospital, enrolled between January 1, 2016, and December 31, 2020, were included in the study. We analyzed the relationship between visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), total adipose tissue (TAT), and skeletal muscle (SM) and 30-day mortality in patients infected with carbapenem-resistant K. pneumoniae (CRKP) in the pulmonary region. Furthermore, we established Cox regression models and a personalized nomogram model to predict the probability of 30-day mortality in these infected patients.

Individuals with high VAT exhibited a higher likelihood of 30-day all-cause mortality (P<0.01) and 30-day mortality due to CRKP infection (P<0.01) compared to those with low VAT. Similar results were observed for TAT. After adjusting for significant comorbidities and other clinical characteristics, Cox regression analysis revealed that male gender (adjusted HR = 4.37; 95% CI = 0.96-19.92, P=0.06), vasopressor use (adjusted HR = 3.65; 95% CI = 1.04-12.85, P=0.04), and VAT (adjusted HR = 1.16; 95% CI = 1.01-1.34, P=0.03) were independent risk factors for 30-day all-cause mortality among these infectious patients.

The study results highlight the significant prognostic value of CT-quantified visceral adipose tissue in patients with CRKP pulmonary infection. Individuals with high VAT are more prone to mortality within 30 days compared to those with low VAT.

The aim of this study was to comprehensively compare the predictive effect of 10 body fat indexes on MAFLD in different sex, age and BMI subgroups.

A total of 5403 physical examination data were included and divided into the MAFLD group (N=2632) and non-MAFLD group (N=2771). The differences and correlation of 10 promising indicators between the two groups were compared, including fatty liver index (FLI), hepatic steatosis index (HSI), lipid accumulation product (LAP), visceral fat index (VAI), cardiometabolic index (CMI), body adiposity index (BAI), and triglyceride-glucose index (TyG), waist circumference index (WC), body mass index (BMI), waist to height ratio (WHtR). Logistic regression was used to analyze the risk of MAFLD under different adjustment conditions. The operating characteristic curve of different genders, BMI levels and age subgroups was plotted.

Male gender, smoking, alcohol drinking, and higher age are risk factors for MAFLD. In addition to BAI, the other 9 indicators had a high correlation with MAFLD, the area under the curve (AUC) value was >0.7, and the prediction effect was better in females, BMI<24 kg/m2, age <35 years subgroup, among which FLI (AUC: 0.912, 95% CI: 0.905-0.920), LAP (AUC: 0.894, 95% CI: 0.8866-0.903), and HSI (AUC: 0.881, 95% CI: 0.872-0.890) have better prediction effects.

Our study confirmed the accuracy of body fat-related indexes in predicting MAFLD in people of different sexes, ages, and BMI levels. Among them, FLI, LAP and HSI have high predictive value and can be utilized as simple and cost-effective tools for screening MAFLD in clinical settings.

Metabolic syndrome (MS), a cluster of cardiometabolic disorders, and sexual dysfunction are two conditions that impact a large proportion of the general population. Although they can occur independently, they are frequently linked and significantly affect people's quality of life. In recent years, research has increasingly focused on the importance of diet, particularly the Mediterranean diet (MD), in modulating sexual function due to its anti-inflammatory, antioxidant, and vasodilatory properties. In this narrative review, we examined the relationship between MS and sexual function in both men and women, with a special emphasis on the MD's therapeutic efficacy in improving sexual dysfunction. In men, MD has been shown to ameliorate erectile dysfunction, as well as several sperm parameters, perhaps leading to improved fertility. On the other hand, adherence to MD has been demonstrated to partially recover several sexual dysfunctions in women, such as those related to their menstrual cycle, menopause, endometriosis, and polycystic ovary syndrome. These favorable effects of MD have been demonstrated in both sexes also among people affected by MS. However, more targeted studies are needed to validate these data for different dietary approaches as well.

Iron deposition and myelin loss are observed in the brain with aging, and iron accumulation is suggested to be involved in myelin damage. However, the exact mechanism of iron deposition with aging remains unclear. This study was aimed to determine whether expanded visceral adipose tissue contributes to iron deposition and myelin loss by inducing hepcidin in the brains of aged male mice. Compared with young adult mice, levels of hepcidin in the brain, epididymal adipose tissue, and circulation were increased in aged mice, which had expanded visceral adipose tissue with inflammation. An increase in expressions of ferritin, an indicator of intracellular iron status, was accompanied by decreased levels of proteins related to myelin sheath in the brains of aged mice. These age-related changes in the brain were improved by visceral fat removal. In addition, IL-6 level, activation of microglia/macrophages, and nuclear translocation of phosphorylated Smad1/5 (pSmad1/5) inducing hepcidin expression were reduced in the brains of aged mice after visceral fat removal, accompanied by decreases of pSmad1/5- and ferritin-positive microglia/macrophages and mature oligodendrocytes. These findings indicate that visceral adiposity contributes to hepcidin-mediated iron deposition and myelin loss with inflammation in the aged brain. Our results support the importance of preventing visceral adiposity for maintaining brain health in older individuals.

Severe burn injuries are defined by a prolonged hypermetabolic response characterized by increases in resting energy expenditure, systemic catabolism, and multi-organ dysfunction. The sustained elevation of catecholamines following a burn injury is thought to significantly contribute to this hypermetabolic response, leading to changes in adipose tissue such as increased lipolysis and the browning of subcutaneous white adipose tissue (WAT). Failure to mitigate these adverse changes within the adipose tissue has been shown to exacerbate the post-burn hypermetabolic response and lead to negative outcomes. Propranolol, a non-selective β-blocker, has been clinically administered to improve outcomes of pediatric and adult burn patients, but there is inadequate knowledge of its effects on the distinct adipose tissue depots. In this study, we investigated the adipose depot-specific alterations that occur in response to burn injury. Moreover, we explored the therapeutic effects of β-adrenoceptor blockade via the drug propranolol in attenuating these burn-induced pathophysiological changes within the different fat depots. Using a murine model of thermal injury, we show that burn injury induces endoplasmic reticulum (ER) stress in the epididymal (eWAT) but not in the inguinal (iWAT) WAT depot. Conversely, burn injury induces the activation of key lipolytic pathways in both eWAT and iWAT depots. Treatment of burn mice with propranolol effectively mitigated adverse burn-induced alterations in the adipose by alleviating ER stress in the eWAT and reducing lipolysis in both depots. Furthermore, propranolol treatment in post-burn mice attenuated UCP1-mediated subcutaneous WAT browning following injury. Overall, our findings suggest that propranolol serves as an effective therapeutic intervention to mitigate the adverse changes induced by burn injury, including ER stress, lipotoxicity, and WAT browning, in both adipose tissue depots. KEY MESSAGES: Burn injury adversely affects adipose tissue metabolism via distinct changes in both visceral and subcutaneous adipose depots. Propranolol, a non-selective β-adrenergic blocker, attenuates many of the adverse adipose tissue changes mediated by burn injury.

The lipid accumulation product (LAP) and the visceral adiposity index (VAI) are suggested as dependable measures for assessing visceral fat levels. Prediabetes is recognized as a condition that precedes the potential onset of diabetes. The objective of this research is to investigate how VAI and LAP are related to prediabetes among the adult population in the United States.

Information from the 2007-2020 National Health and Nutrition Examination Survey (NHANES) was scrutinized in a cross-sectional study. To evaluate the connection between VAI or LAP and the presence of prediabetes, both univariate analysis and multivariate logistic regression were utilized. Threshold effect analysis and fitted smoothing curves were used to delve into the non-linear association between VAI or LAP and prediabetes. Additional analyses were performed on specific subgroups, along with tests to explore potential interactions.

In general, 12,564 American adults were included. After full adjustment, prediabetes with VAI (OR: 1.128, 95% CI: 1.073-1.185) or LAP (OR: 1.006, 95% CI: 1.004-1.008) showed a positive correlation. Individuals in the 4th VAI quartile group faced a significant 61.9% elevated risk for prediabetes (OR: 1.619, 95% CI: 1.354-1.937) when contrasted to those in the 1st VAI quartile. Participants in the 4th LAP quartile group had a significant 116.4% elevated risk for prediabetes (OR: 2.164, 95% CI: 1.747-2.681) when contrasted to individuals of the 1st LAP quartile. Smooth curve fitting analysis revealed a nonlinear correlation of VAI or LAP and prediabetes, and threshold effect analysis was used to determine an inflection point of 4.090 for VAI and 68.168 for LAP.

The values of VAI and LAP are positively associated with the prevalence of prediabetes. The VAI and LAP indices may be used as predictors of prediabetes.

Obesity is a global issue, the development of which depends on many interacting factors. Among these, hormones secreted in the gastrointestinal tract play an important role. The aim of this review was to assess the impact of these hormones on the functions of adipose tissue.

The analysis was based on the latest research concerning both adipose tissue and gastrointestinal hormones.

It was found that these hormones can significantly affect adipose tissue, both directly and indirectly. Some hormones, when secreted in excess, can stimulate adipose tissue formation processes, while others can inhibit them. The impact of hormones depends on the location and type of adipose tissue as well as the physiological state of the body. It should also be noted that no hormone acts in isolation but in close cooperation with other factors.

The relationship between gastrointestinal hormones and adipose tissue, and their role in obesity, is a complex and evolving field of study. Further research is necessary, particularly into the interactions between hormones and other factors, as well as their mutual interactions.