OBJECTIVE: The study was designed to test the effect of anti-diabetic agent pioglitazone and Endothelin-1 (ET-1) on adiponectin secretion from human adipose tissue in depot dependent manner. METHODS: Subcutaneous adipose tissue (SAT) and omental adipose tissues (OAT) were obtained from 19 subjects, including 6 non-obese controls, 7 obese and 6 obese T2DM patients. Adipose tissue was treated with pioglitazone and ET1. Adiponectin secreted into the culture medium after treatment at different time interval (0, 24, 48, 96 hours) was determined by ELISA and normalized for cellular DNA content. RESULTS: Basal adiponectin secretion from both the depots significantly associated with serum adiponectin, BMI, waist and HOMA-IR. Though no depot-specific difference was found in adiponectin secretion from SAT and OAT in our population, significant reduction in adiponectin secretion was observed in SAT of obese and T2DM patients compared to controls. Responsiveness to pioglitazone treatment was more in SAT, while ET1 inhibits adiponectin secretion in OAT. CONCLUSION: These data suggest that, SAT, appears to be major contributor to regulation of adiponectin in circulation. Pioglitazone stimulate adiponectin secretion in SAT compared to OAT in diabetic patients while ET-1 inhibiting adiponectin secretion in OAT of diabetic patients. We need to focus on mechanism underlying these regulatory agents mediated stimulation or inhibition of adiponectin secretion in human adipose tissue.
OBJECTIVE: The study was designed to test the effect of anti-diabetic agent pioglitazone and Endothelin-1 (ET-1) on adiponectin secretion from human adipose tissue in depot dependent manner. METHODS: Subcutaneous adipose tissue (SAT) and omental adipose tissues (OAT) were obtained from 19 subjects, including 6 non-obese controls, 7 obese and 6 obese T2DM patients. Adipose tissue was treated with pioglitazone and ET1. Adiponectin secreted into the culture medium after treatment at different time interval (0, 24, 48, 96 hours) was determined by ELISA and normalized for cellular DNA content. RESULTS: Basal adiponectin secretion from both the depots significantly associated with serum adiponectin, BMI, waist and HOMA-IR. Though no depot-specific difference was found in adiponectin secretion from SAT and OAT in our population, significant reduction in adiponectin secretion was observed in SAT of obese and T2DM patients compared to controls. Responsiveness to pioglitazone treatment was more in SAT, while ET1 inhibits adiponectin secretion in OAT. CONCLUSION: These data suggest that, SAT, appears to be major contributor to regulation of adiponectin in circulation. Pioglitazone stimulate adiponectin secretion in SAT compared to OAT in diabeticpatients while ET-1 inhibiting adiponectin secretion in OAT of diabeticpatients. We need to focus on mechanism underlying these regulatory agents mediated stimulation or inhibition of adiponectin secretion in human adipose tissue.