Antilipolytic Effect of Insulin in Non‐insulin‐dependent Diabetes Mellitus after Conventional Treatment with Diet and Sulfonylurea

Abstract

Insulin-induced antilipolysis was investigated in fat cells obtained after an overnight fast and 60 min after glucose ingestion in seven non-obese patients with non-insulin-dependent diabetes mellitus (NIDDM). The study was performed before and after long-term therapy with diet and glibenclamide. After treatment, the antilipolytic potency of insulin in fat cells was threefold enhanced (p less than 0.05) in the fasting state and remained unaltered after glucose ingestion. In untreated NIDDM oral glucose induced a significant (p less than 0.01) increase in insulin sensitivity. In consequence, in the glucose-fed state insulin sensitivity was similar before and after therapy. Adipocyte insulin receptor binding was comparable before and after therapy, both in the fasting state and following glucose intake. In untreated NIDDM, despite relative hypoinsulinemia, plasma glycerol was markedly reduced after oral glucose. After therapy, plasma glycerol was significantly reduced both in the fasting state and following glucose ingestion. At the same time, fasting and glucose-stimulated circulating insulin were significantly (p less than 0.01) increased. It is concluded that conventional antidiabetes therapy in NIDDM mediates a suppression of adipose tissue lipolysis. This seems to be due to an improvement in insulin secretion in combination with a potentiation of the antilipolytic effectiveness of insulin in fat cells in the fasting state, the latter being secondary to post-binding alterations in insulin action.