ABSTRACT
Clinical and experimental data indicate that there is an increase in plasma FFA levels in type II diabetes. Despite the enhanced lipolysis all evidences suggested no rate of entry of FFA into plasma, implying a compensatory increase in re-esterification of FFA liberated from adipose tissue, a reduced clearance being the most likely explanation for the increase in plasma FFA in NIDDM. The increased FFA availability can impair insulin-mediated glucose disposal and increase hepatic glucose production probably mediated by gluconeogenesis. Finally, while the incresed FFA levels induce insulin resistance in peripheral tissues, particularly muscle, there is a stimulation of insulin secretion in order to match the insulin resistance. However, the chronic FFA overload impairs the B-cells and the hyperinsulinemia no longer matches the increase in insulin resistance and NIDDM begins.