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Gastrointestinal hormones are involved in regulation of glucose metabolism and satiety. We tested the acute effect of meal composition on these hormones in three population groups. A randomized crossover design was used to examine the effects of two energy- and macronutrient-matched meals: a processed-meat and cheese (M-meal) and a vegan meal with tofu (V-meal) on gastrointestinal hormones, and satiety in men with type 2 diabetes (T2D, n = 20), obese men (O, n = 20), and healthy men (H, n = 20). Plasma concentrations of glucagon-like peptide -1 (GLP-1), amylin, and peptide YY (PYY) were determined at 0, 30, 60, 120 and 180 min. Visual analogue scale was used to assess satiety. We used repeated-measures Analysis of variance (ANOVA) for statistical analysis. Postprandial secretion of GLP-1 increased after the V-meal in T2D (by 30.5%; 95%CI 21.2 to 40.7%; p < 0.001) and H (by 15.8%; 95%CI 8.6 to 23.5%; p = 0.01). Postprandial plasma concentrations of amylin increased in in all groups after the V-meal: by 15.7% in T2D (95%CI 11.8 to 19.6%; p < 0.001); by 11.5% in O (95%CI 7.8 to 15.3%; p = 0.03); and by 13.8% in H (95%CI 8.4 to 19.5%; p < 0.001). An increase in postprandial values of PYY after the V-meal was significant only in H (by 18.9%; 95%CI 7.5 to 31.3%; p = 0.03). Satiety was greater in all participants after the V-meal: by 9% in T2D (95%CI 4.4 to 13.6%; p = 0.004); by 18.7% in O (95%CI 12.8 to 24.6%; p < 0.001); and by 25% in H (95%CI 18.2 to 31.7%; p < 0.001). Our results indicate there is an increase in gut hormones and satiety, following consumption of a single plant-based meal with tofu when compared with an energy- and macronutrient-matched processed-meat meat and cheese meal, in healthy, obese and diabetic men.

Adipose tissue (AT) lies at the crossroad of nutrition, metabolism, and immunity; AT inflammation was proposed as a central mechanism connecting obesity with its metabolic and vascular complications. Resident immune cells constitute the second largest AT cellular component after adipocytes and as such play important roles in the maintenance of AT homeostasis. Obesity-induced changes in their number and activity result in the activation of local and later systemic inflammatory response, marking the transition from simple adiposity to diseases such as type 2 diabetes mellitus, arterial hypertension, and ischemic heart disease. This review has focused on the various subsets of immune cells in AT and their role in the development of AT inflammation and obesity-induced insulin resistance., (© 2014 Society for Endocrinology.)

Objectives: The influence of body fat reduction on adipocyte fatty acid-binding protein (A-FABP) in obese patients with type 1 diabetes mellitus (T1DM) was investigated to examine whether it relates to the etiopathogenesis of insulin resistance (IR) and obesity., Methods: We studied 14 obese patients with T1DM and IR (42.6±9.4 years, BMI 32.4±2.1 kg/m2) and 13 non-obese control patients with T1DM (36.9±13.9 years, BMI 22.6±2.1 kg/m2). Plasma FABP was measured by ELISA and plasma free fatty acids (FFA) were measured spectrophotometrically before weight reduction, immediately after 7 days of fasting and after 21 days on a low-calorie diet. The control group was studied only after overnight fasting. Body composition was examined using bioimpedance spectroscopy. The means ± SD, T-test, one-way ANOVA and Spearman's correlation were used for statistical evaluation., Results: All patients tolerated the period of fasting. Obese T1DM patients lost 6.1±1.1 kg. There was a significant decrease in body mass index and body fat measured 21 days after weight reduction (p<0.05). Plasma FABP and FFA concentrations in obese T1DM patients before weight reduction were significantly higher than in controls, further increased significantly after fasting (p<0.05) and were restored thereafter. Significant positive correlations between FABP and FFA and between FABP and BMI (p<0.05) were found., Conclusion: Increased plasma FABP indicates insulin resistance in obese patients with T1DM. Weight reduction in T1DM patients is associated with a desirable decrease of body fat and transiently increased FABP. This increase might be a temporary adaptation of metabolism to non-stress fasting.

Objective: We have assessed in obese renal transplant recipients a course of selected proinflammatory factors liable to influence the long-term outcome of transplant patients and kidney grafts., Design and Patients: In a prospective cohort study, we examined a total of 68 obese renal transplant recipients (body mass index [BMI] >or= 30 kg/m(2)) for a period of 12 months (Group I). A control group consisted of 72 comparable non-obese renal transplant recipients (Group II)., Results: Significant differences were found in plasma 12 months after renal transplantation (Group I versus Group II) in asymmetric dimethylarginine (ADMA; 3.68 micromol/L +/- 0.42 micromol/L vs 2.10 micromol/L +/- 0.34 micromol/L; P < .01), adiponectin (ADPN; 15.1 microg/mL +/- 6.0 microg/mL vs 22.80 microg/mL +/- 7.2 microg/mL; P < .01), leptin (50.4 ng/L +/- 10.2 ng/L vs 22.0 ng/L +/- 8.4 ng/L; P < .01), solubile leptin receptor (ObRe; 23.6 U/mL +/- 7.4 U/mL vs 47.2 U/mL +/- 10.7 U/mL; P < .01), resistin (21.2 microg/mL +/- 10.2 microg/mL vs 15.0 microg/mL +/- 6.2 microg/mL; P < .025) and triglycerides (3.9 mmol/L +/- 1.6 mmol/L vs 2.8 mmol/L +/- 1.6 mmol/L; P < .01). There were significant correlations between ADMA and BMI (r = 0.525, P < .001), ADPN and BMI (r = -0.574, P < .001), and ADMA and ADPN in visceral fat (r = -0.510, P < .001). Correlation between ADMA and Cin was weak, but significant (r = -0.190, P < .05)., Conclusion: The results indicate that obesity after renal transplantation was associated with increased plasma ADMA and decreased ADPN in plasma and in fat tissue and may represent a risk factor for renal transplant recipients.

Background: In obese renal transplant recipients, we assessed the course of selected proinflammatory factors liable to influence long-term outcomes of transplant patients and kidney grafts., Methods: In a prospective cohort study, we examined a total of 140 renal transplant recipients for a period of 12 months. Based on body mass index (BMI), patients were divided into Group I (BMI > or = 30 kg/m2, 68 patients) and Group II (BMI < or = 30 kg/m2, 72 patients)., Results: Twelve months after renal transplantation, significant differences were found between Group I versus Group II in plasma levels of asymmetric dimethylarginine (ADMA) (3.65 [SD +/- 0.47 micromol/L] versus 2.01 [SD +/- 0.36 micromol/L], P < .01), adiponectin (ADPN) (15.4 [SD +/- 6.6 microg/mL] versus 22.3 [SD +/- 8.2 microg/mL], P < .01), leptin (51.3 [SD +/- 11.2 ng/L] versus 21.3 [SD +/- 9.2 ng/L], P < .01), soluble leptin receptor (24.6 [SD +/- 8.4 U/mL] versus 46.1 [SD +/- 11.4 U/mL], P < .01), resistin (20.8 [SD +/- 10.1 microg/mL] versus 14.6 [SD +/- 6.4 microg/mL], P < .025), and triglycerides (3.9 [SD +/- 1.6] versus mmol/L 2.8 [SD +/- 1.6 mmol/L], P < .01). There were significant correlations between ADMA and BMI (r = 0.520; P < .001), and ADPN and BMI (r = -0.570, P < .001). The correlation between ADMA and inulin clearance (Cin) was weak (r = -0.185, P < .05)., Conclusions: Obesity after renal transplantation is associated with increased ADMA and decreased ADPN in plasma, and this may represent a risk factor for renal transplant recipients.

Resistin is a 12.5-kDa polypeptide hormone produced by adipocytes and immunocompetent cells. It was originally proposed as a link between obesity and insulin resistance/diabetes. Later, studies revealed that substantial inter-species differences exist between the major sites of resistin production in rodents (adipocytes) and humans (immunocompetent cells). While in rodents resistin appears to have an important role in the development of liver insulin resistance, its role in humans is less clear, and it is probably involved in the regulation of inflammatory processes rather than in insulin sensitivity. Current experimental and clinical data concerning resistin physiology and pathophysiology, and its possible role in the development of insulin resistance and atherosclerosis are detailed in this review.

Adiponectin is a protein hormone produced exclusively by adipocytes. Its circulating levels are decreased in individuals with obesity, atherosclerosis and insulin resistance, suggesting that its deficiency may have a causal role in the etiopathogenesis of these diseases. Studies have shown that adiponectin administration in rodents has insulin-sensitizing, anti-atherogenic and anti-inflammatory effects and under certain settings also decreases body weight. Therefore, adiponectin replacement in humans may represent a promising approach to prevent and/or treat obesity, insulin resistance and type 2 diabetes; however, clinical studies with adiponectin administration need to be conducted to confirm this hypothesis. Current experimental and clinical data regarding adiponectin physiology and pathophysiology are detailed in this review.

We studied the effects of genetic background on the phenotype of ob/ob mice, a model of severe obesity, insulin resistance, and diabetes caused by leptin deficiency. Despite a comparable degree of obesity and hyperinsulinemia, C57BL/6J ob/ob mice had much milder hyperglycemia and, surprisingly, normal circulating adiponectin levels despite still-prominent signs of insulin resistance. Hyperinsulinemic-euglycemic clamp revealed relatively less whole-body and muscle insulin resistance in C57BL/6J ob/ob mice, whereas liver insulin resistance tended to be more severe than in FVB/N ob/ob mice. C57BL/6J ob/ob mice had also more rapid clearance of circulating triglycerides and more severe hepatic steatosis. We suggest that strain-related distinction in lipid handling is the most important player in the differences in diabetic phenotype and insulin sensitivity, whereas the impact of circulating adiponectin levels on the overall phenotype of ob/ob mice is less important.

A study published in the European Heart Journal explores the effects of dapagliflozin, a sodium-glucose cotransporter 2 inhibitor (SGLT2i), on weight loss in patients with heart failure with preserved ejection fraction (HFpEF). The study found that dapagliflozin treatment resulted in greater weight loss in obese individuals compared to lean individuals, with most of the weight loss being fat rather than water or lean tissue. The study also discovered that dapagliflozin increased levels of peptide YY (PYY), a hormone that promotes satiety and decreases appetite. The increase in PYY was correlated with weight loss, particularly in adipose tissue, and favorable haemodynamic effects during exercise. These findings suggest that SGLT2i-mediated increases in PYY may contribute to weight loss in obese HFpEF patients through increased satiety, with secondary haemodynamic benefits. [Extracted from the article]

Diabetes is a disease of great and rising prevalence, with the obesity epidemic being a significant contributing risk factor. Duodenal–jejunal bypass liner (DJBL) is a reversible implant that mimics the effects of more aggressive surgical procedures, such as gastric bypass, to induce weight loss. We hypothesized that DJBL also influences the glucose dynamics in type II diabetes, based on the induced changes already demonstrated in other physiological characteristics and parameters. In order to assess the validity of this assumption, we conducted a quantitative analysis based on several nonlinear algorithms (Lempel–Ziv Complexity, Sample Entropy, Permutation Entropy, and modified Permutation Entropy), well suited to the characterization of biomedical time series. We applied them to glucose records drawn from two extreme cases available of DJBL implantation: before and after 10 months. The results confirmed the hypothesis and an accuracy of 86.4% was achieved with modified Permutation Entropy. Other metrics also yielded significant classification accuracy results, all above 70%, provided a suitable parameter configuration was chosen. With the Leave–One–Out method, the results were very similar, between 72% and 82% classification accuracy. There was also a decrease in entropy of glycaemia records during the time interval studied. These findings provide a solid foundation to assess how glucose metabolism may be influenced by DJBL implantation and opens a new line of research in this field. [ABSTRACT FROM AUTHOR]

In this Article, the author reflects on accumulation of adipose tissue that increases the risk of insulin resistance, Type 2 diabetes, dyslipidemia, arterial hypertension, several types of cancer and much other co-morbidity. Evidence on mice reveals that leptin levels correlates with the body fat content, could be used for clinical use. It further states that Thiazoli-dinediones is the only available drug which partially inhibits inflammation in adipose tissue.