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u able to sustain the magnitude of compensatory hyperinsulinemia needed to prevent gross decompensation of glucose tolerance.

As commonly used, the phrase ''insulin resistance'' refers to a decrease in the ability of a defined amount of insulin to stimulate glucose disposal by muscle. However, there is no accepted criterion that permits a precise definition of the magnitude of the defect in insulin-stimulated glucose disposal by muscle that provides the means to designate a person as ''insulin sensitive'' or ''insulin resistant.'' Instead, as shown in Figure 1, insulin-stimulated glucose disposal rates in nondiabetic individuals vary continuously from the most insulin-sensitive to the most insulin-resistant individual, and the best we can do is to understand that the more insulin-resistant an individual, the more at risk they are of developing one or more of the manifestations of syndrome X. The variability of insulin-stimulated glucose disposal is 490 healthy volunteers is shown in Figure 1. These measurements were made with the insulin suppression test, an approach to quantify insulin-mediated glucose disposal by determining the steady-state plasma insulin (SSPI) and steady-state plasma glucose (SSPG) concentrations achieved during the last 30 min of a continuous infusion of octreotide, insulin, and glucose. The octreotide infusion suppresses endogenous insulin secretion, and the exogenous insulin infusion produces a steady-state level of physiological hyperinsuli-nemia. Because the SSPI concentration is similar for all subjects, the SSPG concentration provides a direct measure of the ability of insulin to mediate disposal of an infused glucose load; the higher the SSPG concentration, the more insulin resistant the individual.

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