Insulin-Stimulated Glucose Disposal in Patients with Type I (IDDM) and Type II (NIDDM) Diabetes Mellitus
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In 1933 Himsworth and Kerr8 used the plasma glucose response to an oral glucose plus intravenous insulin challenge to divide patients with diabetes mellitus into two types — designated as being either insulin sensitive or insulin insensitive. Based upon the available clinical information, patients classified by Himsworth as being insulin sensitive seem most comparable to individuals who would be designated as having insulin-dependent diabetes (IDDM) by today’s criteria.12 In contrast, the group of patients who would be classified today as having noninsulin-dependent diabetes mellitus (NIDDM) share the characteristics of those designated by Himsworth as being insulin insensitive. Several years ago,16 we reviewed available information as to the ability of insulin to stimulate glucose uptake in patients with diabetes mellitus. At that time we indicated that resistance to insulin-stimulated glucose uptake characterizes patients with NIDDM, but that it could also exist in patients with IDDM. However, in the latter instance the resistance appeared to be related to degree of metabolic control, and it seemed to us that insulin sensitivity was normal in patients with IDDM well-controlled on insulin. Interest in the role played by insulin resistance in the pathogenesis of diabetes mellitus has increased greatly since publication of our earlier review. This has been associated with the development of new techniques for the assessment of insulin-stimulated glucose uptake in patients with diabetes, resulting in the appearance of a considerable amount of new information as to the characteristics of insulin action in patients with both NIDDM and IDDH. The purpose of this presentation will be to critically review available data, and to use this information in an attempt to define the effects of IDDH and NIDDH on insulin-stimulated glucose disposal.
KeywordsInsulin Resistance Insulin Action Continuous Subcutaneous Insulin Infusion Insulin Deficiency Stimulate Glucose Uptake
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