Short-term effects of obestatin on hexose uptake and triacylglycerol breakdown in human subcutaneous adipocytes

AIM To study complete dose-dependent effects of obestatin on lipolytic and glucose transport activities in human adipocyte preparations highly responsive to insulin.METHODS Adipocytes were prepared by liberase digestion from subcutaneous abdominal adipose tissue obtained from overweight subjects undergoing plastic surgery. The index of lipolytic activity was the glycerol released in the incubation medium, while glucose transport was assessed by [~3H]-2-deoxyglucose uptake assay.RESULTS When tested from 0.1 nmol/L to 1 μmol/L, obestatin did not stimulate glycerol release; it did not inhibit the lipolytic effect of isoprenaline and did not alter the insulin antilipolytic effect. Obestatin hardly activated glucose transport at 1 μmol/L only. Moreover, the obestatin stimulation effect was clearly lower than the threefold increase induced by insulin 100 nmol/L.CONCLUSION Low doses of obestatin cannot directly influence lipolysis and glucose uptake in human fat cells.

Hyperglycemia and reduced adiposity of streptozotocin-induced diabetic mice are not alleviated by oral benzylamine supplementation

BACKGROUND Benzylamine(Bza)oral administration delays the onset of hyperglycemia in insulin-resistant db-/-mice;a genetic model of obesity and type 2 diabetes.AIM To extend the antihyperglycemic properties of oral benzylamine to a model of insulin-deficient type 1 diabetes.METHODS Male Swiss mice were rendered diabetic by streptozotocin treatment(STZ)and divided in two groups:one received 0.5%Bza as drinking solution for 24 d(STZ Bza-drinking)while the other was drinking water ad libitum.Similar groups were constituted in age-matched,nondiabetic mice.Food intake,liquid intake,body weight gain and nonfasting blood glucose levels were followed during treatment.At the end of treatment,fasted glycemia,liver and white adipose tissue(WAT)mass were measured,while glucose uptake assays were performed in adipocytes.RESULTS STZ diabetic mice presented typical features of insulin-deficient diabetes:reduced body mass and increased blood glucose levels.These altered parameters were not normalized in the Bza-drinking group in spite of restored food and water intake.Bza consumption could not reverse the severe fat depot atrophy of STZ diabetic mice.In the nondiabetic mice,no difference was found between control and Bza-drinking mice for any parameter.In isolated adipocytes,hexose uptake was partially activated by 0.1 mmol/L Bza in a manner that was obliterated in vitro by the amine oxidase inhibitor phenelzine and that remained unchanged after Bza supplementation.Oxidation of 0.1 mmol/L Bza in WAT was lower in STZ diabetic than in normoglycemic mice.CONCLUSION Bza supplementation could not normalize the altered glucose handling of STZ diabetic mice with severe WAT atrophy.Consequently,its antidiabetic potential in obese and diabetic rodents does not apply to lipoatrophic type 1 diabetic mice.