Insulin Secretion in Diabetes Mellitus
- DAVID M. KIPNIS, M.D., F.A.C.P.
- Requests for reprints should be addressed to David M. Kipnis, M.D., Metabolism Division, Department of Medicine, Washington University School of Medicine, St. Louis, Mo. 63106.
SUMMARY
Measurements of the plasma immunoreactive insulin responses to various insulinogenic stimuli in prediabetic, latent, juvenile, and maturity-onset diabetics indicate that impaired insulin secretion is a characteristic feature of the diabetic state. The development of overt diabetes depends, however, on both the degree of impairment of insulin secretion and the insulin sensitivity of the individual. The maintenance of normal carbohydrate tolerance in preand latent diabetics, despite decreased insulin secretion, indicates increased endorgan responsiveness to insulin.
Normal-weight, maturity-onset diabetics also exhibit increased glucose utilization per unit insulin secreted, but insulin secretion is sufficiently impaired to result in overt diabetes. In these terms conditions that increase insulin resistance—obesity, pregnancy, infection, excess glucocorticoids, and growth hormone—precipitate, and conditions that decrease insulin resistance—for example, glucocorticoid and growth hormone deficiency and unknown factors—delay the onset of overt diabetes in individuals possessing the inherited beta cell defect characteristic of diabetes mellitus.
Article and Author Information
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From the Metabolism Division, Department of Medicine, Washington University School of Medicine, St. Louis, Mo.
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This study was supported in part by grants AM-1921, AM-5105, and FR-36, U. S. Public Health Service, Washington, D. C.
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- Received June 14, 1968.
- Accepted June 24, 1968.
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