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Cited by 317Pancreatic function and diabetesDiabetes and associated disordersAdrenal Hormones and Disorders

Therapeutic effects of dehydroepiandrosterone (DHEA) in diabetic mice.

Coleman, D L, Leiter, E H, Schwizer, R W·1982·Diabetes
DOI 10.2337/diab.31.9.830
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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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  • The 70-95% reduction in formation of DHEA and DHEA-S by the adrenals during aging results in a dramatic reduction in formation of androgens and estrogens in peripheral target tissues, which could be involved in pathogenesis of age-related diseases such as insulin resistance and obesity.

    “The 70 -95% reduction in the formation of DHEA and DHEA-S by the adrenals during aging results in a dramatic reduction in the formation of androgens and estrogens in peripheral target tissues, which could well be involved in the pathogenesis of age-related diseases such as insulin resistance (307, 308) and obesity (309 -311).”

    From Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone (2003) · cites this paper as [308]

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Authors
Coleman, D. L., Leiter, E. H., & Schwizer, R. W.
Affiliations
Jackson Laboratory (US)
ORCID
Coleman, D L
Venue
Diabetes
Publisher
American Diabetes Association
Published
1982-09-01
Volume
31
Issue
9
Pages
830-833
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diab.31.9.830
OpenAlex
W1998106197
Cited by
317
References
0
Citations by year
2026: 1 · 2023: 2 · 2022: 7 · 2020: 2 · 2019: 2 · 2018: 4 · 2016: 8 · 2015: 6 · 2014: 5 · 2013: 3 · 2012: 8
FWCI
9.70
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
  • The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
dehydroepiandrosterone, type 2 diabetes, type 1 diabetes, db/db mice, streptozotocin-induced diabetes, insulin resistance, beta-cell function, beta cell necrosis, islet atrophy, hyperglycemia, impaired glucose tolerance, obesity, insulitis, plasma insulin, glucocorticoids
MeSH terms
Animals, Blood Glucose, Dehydroepiandrosterone, Diabetes Mellitus, Experimental, Female, Male, Mice, Inbred C57BL, Pancreas, Mice

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