Abstract
Non–insulin-dependent diabetes mellitus (NIDDM) is characterized by increased hepatic glucose production and deficient peripheral glucose uptake. 1 These disturbances in glucose metabolism are thought to result from cellular resistance to insulin action and deficient secretion of insulin. 2,3 The cellular resistance to insulin action is caused by disturbances in one or more postreceptor sites of insulin action. 4,5 Decrease in insulin binding does occur, but it is thought to be due to down-regulation of the insulin receptor secondary to the increased basal plasma insulin levels. 5 A small direct decrease in insulin receptors in NIDDM cannot be excluded as a contributory cause to the insulin resistance. The β cell in patients with NIDDM does not secrete insulin appropriately in response to glucose. 3 This abnormality is likely the result of an intracellular disturbance and results in delayed as well as insufficient glucose-mediated insulin secretion. 6 As the level of fasting hyperglycemia increases, β-cell glucose-mediated insulin
Published Version
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