Reduced insulin-mediated glucose uptake, or insulin resistance, is a metabolic defect characteristic of virtually all patients with non-insulin-dependent diabetes mellitus (NIDDM). The cause of insulin resistance remains unknown, but in the past decade, since the development of the hyperinsulinemic-glucose-clamp technique, considerable progress has been made in identifying the insulin-resistant tissues and metabolic pathways responsible for decreased insulin action. DeFronzo et al.1 , 2 and subsequently others demonstrated that most of the glucose that leaves the plasma during hyperinsulinemia enters peripheral tissues rather than the gut or liver, and that insulin resistance in patients with NIDDM is largely a result of decreased glucose . . .
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Bogardus et al. (1990) studied this question.
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