Faculty Research 1980 - 1989

Therapeutic effects of dehydroepiandrosterone (DHEA) in diabetic mice.

Document Type

Article

Publication Date

1982

Keywords

Blood-Glucose: an, Dehydroepiandrosterone: tu, Diabetes-Mellitus-Experimental: dt, bl, pa, Female, Male, Mice, Mice-Inbred-C57BL, Pancreas: pa, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S

First Page

830

Last Page

833

JAX Location

45,520

JAX Source

Diabetes. 1982 Sep; 31(9):830-3.

Grant

AM14461, AM20725, AM17631

Abstract

Dehydroepiandrosterone (DHEA), a major adrenal secretory steroid in humans, was therapeutic when fed in a concentration of 0.4% to C57BL/KsJ mice with either non-insulin-dependent or insulin-dependent diabetes. Genetically diabetic (db/db) mice of both sexes develop obesity and a glucose intolerance and hyperglycemia associated with insulin resistance by 2 mo of age, and exhibit beta-cell necrosis and islet atrophy by 4 mo. In contrast, DHEA feeding initiated between 1 and 4 mo of age, while only moderately effective in preventing obesity, did prevent the other pathogenic changes and effected a rapid remission of hyperglycemia, a preservation of beta-cell structure and function, and an increased insulin sensitivity as measured by glucose tolerance tests. DHEA feeding was also therapeutic to normal C57BL/KsJ male mice made diabetic by multiple low doses of streptozotocin (SZ). While DHEA treatments did not block either the direct cytotoxic action of SZ on beta-cells or the development of insulitis, the steroid significantly moderated the severity of the ensuing diabetes (reduced hyperglycemia and water consumption, and increased plasma insulin and numbers of residual, granulated beta-cells.

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