Epicardial and pericardial fat in type 2 diabetes: favourable effects of biliopancreatic diversion.

PURPOSE: Ectopic fat is often identified in obese subjects who are susceptible to the development of type 2 diabetes mellitus (T2DM). The ectopic fat favours the decrease in insulin sensitivity (IS) and adiponectin levels. We aimed to evaluate the effect of biliopancreatic diversion (BPD) on the accumulation of ectopic fat, adiponectin levels and IS in obese with T2DM. MATERIALS AND METHODS: A nonrandomised controlled study was performed on sixty-eight women: 19 lean-control (23.0 ± 2.2 kg/m(2)) and 18 obese-control (35.0 ± 4.8 kg/m(2)) with normal glucose tolerance and 31 obese with T2DM (36.3 ± 3.7 kg/m(2)). Of the 31 diabetic women, 20 underwent BPD and were reassessed 1 month and 12 months after surgery. The subcutaneous adipose tissue, visceral adipose tissue, epicardial adipose tissue and pericardial adipose tissue were evaluated by ultrasonography. The IS was assessed by a hyperglycaemic clamp, applying the minimal model of glucose. RESULTS: One month after surgery, there was a reduction in visceral and subcutaneous adipose tissues, whereas epicardial and pericardial adipose tissues exhibited significant reduction at the 12-month assessment (p < 0.01). Adiponectin levels and IS were normalised 1 month after surgery, resembling lean-control values and elevated above the obese-control values (p < 0.01). After 12 months, the improvement in IS and adiponectin was maintained, and 17 of the 20 operated patients exhibited fasting glucose and glycated haemoglobin within the normal range. CONCLUSIONS: After BPD, positive physiological adaptations occurred in grade I and II obese patients with T2DM. These adaptations relate to the restoration of IS and decreased adiposopathy and explain the acute (1 month) and chronic (12 months) improvements in the glycaemic control.

Impaired incretin secretion and pancreatic dysfunction with older age and diabetes.

OBJECTIVE: To estimate the impact of aging and diabetes on insulin sensitivity, beta-cell function, adipocytokines, and incretin production. METHODS: Hyperglycemic clamps, arginine tests and meal tolerance tests were performed in 50 non-obese subjects to measure insulin sensitivity (IS) and insulin secretion as well as plasma levels of glucagon, GLP-1 and GIP. Patients with diabetes and healthy control subjects were divided into the following groups: middle-aged type 2 diabetes (MA-DM), aged Type 2 diabetes (A-DM) and middle-aged or aged subjects with normal glucose tolerance (MA-NGT or A-NGT). RESULTS: IS, as determined by the homeostasis model assessment, glucose infusion rate, and oral glucose insulin sensitivity, was reduced in the aged and DM groups compared with MA-NGT, but it was similar in the MA-DM and A-DM groups. Insulinogenic index, first and second phase insulin secretion and the disposition indices, but not insulin response to arginine, were reduced in the aged and DM groups. Postprandial glucagon production was higher in MA-DM compared to MA-NGT. Whereas the GLP-1 production was reduced in A-DM, no differences between groups were observed in GIP production. CONCLUSIONS: In non-obese subjects, diabetes and aging impair insulin sensitivity. Insulin production is reduced by aging, and diabetes exacerbates this condition. Aging associated defects superimposed diabetic physiopathology, particularly regarding GLP-1 production. On the other hand, the glucose-independent secretion of insulin was preserved. Knowledge of the complex relationship between aging and diabetes could support the development of physiopathological and pharmacological based therapies.

ß-Cell function improvements in grade I/II obese subjects with type 2 diabetes 1 month after biliopancreatic diversion: results from modeling analyses of oral glucose tolerance tests and hyperglycemic clamp studies.

OBJECTIVE: To investigate the effect of biliopancreatic diversion (BPD) surgery on ß-cell function in grade I and II obese patients with type 2 diabetes using oral and intravenous glucose loads. RESEARCH DESIGN AND METHODS: Sixty-eight women were divided into the following three groups: 19 lean-control (23.0 ± 2.2 kg/m(2)) and 18 obese-control (35.0 ± 4.8 kg/m(2)) subjects with normal glucose tolerance, and 31 obese patients with type 2 diabetes (36.3 ± 3.7 kg/m(2)). Of the 31 diabetic women, 64% underwent BPD (n = 20, BMI: 36.5 ± 3.7 kg/m(2)) and were reassessed 1 month after surgery. Oral glucose tolerance tests and hyperglycemic clamps were performed. Mathematical modeling was used to analyze basal and stimulated ß-cell function, insulin sensitivity (IS), hepatic extraction (HE) of insulin, and delay time of ß-cell response to a specific plasma glucose concentration. RESULTS: After BPD, restoration of the basal disposition index (P < 0.001) and improvement of the stimulated disposition indices in oral and intravenous glucose stimulation of the ß-cell were observed (P < 0.05). In both dynamic tests, there were no changes in the delay time of ß-cell response. IS for oral glucose stimulation (IS(oral)) and intravenous clamp glucose stimulation (IS(clamp)) was completely normalized (P < 0.001). IS(oral) and IS(clamp) increased approximately 5.0-fold and 3.5-fold, respectively (P < 0.01). The HE of insulin increased in the basal (P < 0.05) and stimulated states (P < 0.01). CONCLUSIONS: ß-Cell function, IS, and HE of insulin improved after BPD, which improved glycemic control.

Sagittal abdominal diameter as a marker for epicardial adipose tissue in premenopausal women.

OBJECTIVE: Accumulation of epicardial (EAT) adipose tissue is associated with the development of an unfavorable metabolic risk profile. Gold standard methods used to assess this fat depot are not routinely applicable in the clinic. Anthropometric measures, including the sagittal abdominal diameter (SAD), have emerged as surrogate markers of visceral obesity. We determined the relationship between EAT measurement and cardiometabolic risk parameters and the potential use of the SAD, compared with other anthropometric parameters, as a practical estimation of EAT. MATERIALS/METHODS: Sixty-seven premenopausal women were evaluated. The anthropometric parameters that were measured included waist circumference, SAD, body mass index and waist-to-hip ratio. EAT was determined by echocardiogram. Visceral adipose tissue (VAT) was determined by abdominal ultrasound. Insulin sensitivity was assessed by the hyperglycemic clamp. RESULTS: The accumulation of EAT was correlated with impaired insulin sensitivity and decreased adiponectin. All of the anthropometric measurements were correlated with EAT. Interestingly, EAT was most significantly correlated with the SAD. From the ROC analysis, we found that the SAD measurements were very accurate, presenting the highest area under the curve for EAT (0.81; p<0.01) when compared with the other measurements. In the multiple linear regression analysis, EAT was moderately predicted by the SAD (R²=0.25; p<0.001). CONCLUSION: SAD, a simple anthropometric measure, accurately estimated EAT and thus represents a clinically useful non-invasive marker that can identify patients with EAT accumulation.

TyG index performs better than HOMA in a Brazilian population: a hyperglycemic clamp validated study.

The TyG index was evaluated as a surrogate method for estimation of insulin resistance (IR). TyG index correlated with adiposity, metabolic and atherosclerosis markers related to IR and presented a moderate degree of agreement with hyperglycemic clamp. TyG index represents an accessible tool for assessment of IR in clinical practice.