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The Effects of Vitamin A on Insulin Release and Glucose Oxidation in Isolated Rat Islets^*

Section of Endocrinology, Departments of Medicine and Nuclear Medicine, V.A. West Side Hospital and the Abraham Lincoln School of Medicine, University of Illinois College of Medicine Chicago, Illinois 60612

Address requests for reprints to: Bruce S. Chertow, M.D., Huntington VA Hospital, 1540 Spring Valley Drive, Huntington, West Virginia 25701.

Abstract

We tested the effects of vitamin A, a membrane surface-active agent, on glucose (16.7 mM)- induced biphasic insulin release from collagenase-isolated rat islets. Also, efforts were made to correlate the effects of vitamin A with glucose oxidation. Vitamin A (10^-4 M) inhibited first- and second phase insulin release; 10^-5 M vitamin A inhibited second phase release only and to a lesser extent than that observed with 10^-4 M vitamin A; and 10^-6 M vitamin A had no effect. Vitamin A (10^-7 M) stimulated biphasic insulin release. Exposure to high glucose (27.8 mM) overcame the effects of 10^-4 M vitamin A on first phase release, but not on second phase release of insulin. Exposure to 10^-5 M hydrocortisone opposed the effects of 10^-4 M vitamin A on both phases of insulin release.

Vitamin A (10^-4 and 10M^-5 M) inhibited glucose oxidation by islets, as measured by the production of 14CO2 from [¹⁴C]glucose. The effects of vitamin A on insulin release were dissociated in part from those effects on glucose oxidation, in that hydrocortisone opposed the effect of vitamin A on insulin release but not on glucose oxidation.

The effects of vitamin A on insulin secretion can best be explained by the interaction of vitamin A at multiple sites affecting the membrane and intracellular glucose oxidation.

Footnotes

^* These studies were reported in part in abstract form in the Program of the 37th Annual Meeting of the American Diabetes Association (vol. 26, suppl. 1), June, 1977, and were presented in part at the Meeting of the Midwestern Section of the American Federation of Clinical Research on Nov. 3, 1977, Chicago, Illinois. This work was supported in part by the V.A. Research Program (MRIS 1387) and in part by a grant from the American Diabetes Association.

Received July 27, 1977.