Improved glycemic control increases fasting plasma acylation-stimulating protein and decreases leptin concentrations in type II diabetic subjects

Acylation-stimulating protein is an adipocyte-derived protein that has rece ntly been suggested to play an important role in the regulation of triglyce ride storage. To date, little information has been reported with regard to fasting acylation-stimulating protein levels and its relation to metabolic control, leptin, and/or lipids in subjects with diabetes mellitus. We there fore evaluated fasting acylation-stimulating protein, leptin, and lipid lev els before and 4 months after improving glycemic control with sulfonylurea treatment in a group of poorly controlled obese women with type 2 diabetes and in age- and body mass index-matched nondiabetic obese women. Fasting plasma acylation-stimulating protein (49.67 +/- 19.73 vs. 48.49 +/- 20.70 nmol/liter) and leptin concentrations (33.7 +/- 23.2 vs. 26.2 +/- 10 .6 ng/ml) were not significantly different between the groups. Improvement of glycemic control produced parallel falls in fasting blood glucose and he moglobin A(1c). Plasma leptin concentrations were also significantly reduce d (33.69 +/- 23.2 vs. 22.73 +/- 11.26 ng/ml; P = 0.036), whereas fasting ac ylation-stimulating protein concentrations were significantly increased aft er treatment (48.49 +/- 20.70 vs. 72,82 +/- 29,72 nmol/liter; P = 0.004). N evertheless, lipids and apolipoprotein B did not significantly improve. We could not find any correlation between elevated acylation-stimulating prote in levels and changes in body mass index, glucose, insulin, hemoglobin A(1c ), leptin, or lipid levels. Similarly, the decrement in circulating leptin levels observed after treatment did not correlate with changes in the level s of glucose, insulin, hemoglobin A(1c), or any lipid parameters. We conclude that improved glycemic control increases fasting acylation-stim ulating protein and decreases leptin concentrations, but not corrects criti cal lipid abnormalities in type 2 obese diabetic subjects. Moreover, altere d plasma acylation-stimulating protein levels are not associated with chang es in body mass index or lipid, leptin, insulin, or glucose levels. Thus, o ur findings suggest that improved glycemic control or insulin resistance is not responsible for abnormal fatty acid trapping, and failure of lipids to improve after treatment in our patients is consistent with the acylation-s timulating protein resistance concept.