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Review Article
Seminars in Medicine of the Beth Israel Deaconess Medical Center
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Volume 334:777-783 March 21, 1996 Number 12
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Non-Insulin-Dependent Diabetes Mellitus — A Genetically Programmed Failure of the Beta Cell to Compensate for Insulin Resistance
Kenneth S. Polonsky, M.D., Jeppe Sturis, Ph.D., and Graeme I. Bell, Ph.D.

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Non-insulin-dependent diabetes mellitus (NIDDM), the commonest form of diabetes, affects approximately 5 percent of the population of the United States. Although the pathophysiology of this condition has not been fully characterized and the nature of the primary defect is controversial, the results of recent studies provide insights into its basic causes. Here, we review these studies and suggest how insulin resistance and genetically programmed pancreatic beta-cell dysfunction may interact in susceptible persons to cause diabetes.

Insulin Resistance

Insulin resistance is a diminished ability of insulin to exert its biologic action across a broad range of concentrations. Unless persons with insulin resistance secrete . . . [Full Text of this Article]

Insulin Resistance and the Risk of Niddm

The Beta-Cell Response to Insulin Resistance

The Role of Abnormal Beta-Cell Function in the Evolution of Niddm

Studies in Animals

Studies in Humans

            Persons with Overt Diabetes

            Persons with Impaired Glucose Tolerance

            Persons with Normal Plasma Glucose Concentrations

Genetics of Classic Niddm

Discussion


Source Information

From the Departments of Medicine (K.S.P., J.S., G.I.B.), Biochemistry (G.I.B.), and Molecular Biology (G.I.B.) and the Howard Hughes Medical Institute, University of Chicago and Pritzker School of Medicine, Chicago.

Address reprint requests to Dr. Polonsky at the University of Chicago, Dept. of Medicine, 5841 S. Maryland Ave., MC 1027, Chicago, IL 60637.

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