Affiliation:
1. Department of Medicine, Stanford University School of Medicine,
Stanford, California 94305; and Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs Medical Center, Palo Alto, California 94304
Abstract
Resistance to insulin-mediated glucose uptake is characteristic of individuals with impaired glucose intolerance or non-insulin-dependent diabetes, and it also occurs commonliyn patients with high blood pressure. The physiological response to a decrease in insulin-mediated glucose uptake is an increase in insulin secretion, and as long as a state of compensatory hyperinsulinemia can be maintained, frank decompensation of glucose tolerance can be prevented. However, it is likely that the defect in insulin action and/or the associated hyperinsulinemia will lead to an increase in plasma triglyceride and a decrease in high density lipoprotein-cholesterol concentration, and high blood pressure. It seems likely that the cluster of changes associated with resistance to insulin-mediated glucose uptake comprise a syndrome, which plays an important role in the etiology and clinical course of patients with non-insulin-dependent diabetes, high blood pressure, and coronary heart disease.
Subject
General Biochemistry, Genetics and Molecular Biology,General Medicine
Cited by
648 articles.
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