Effect of dehydroepiandrosterone in hereditarily diabetic rats

Goto‐Kakizaki rats (GK rats) were given access for 4 weeks to a diet enriched with dehydroepiandrosterone (DHEA, 0·2 per cent, w/w). The incorporation of DHEA in the food failed to affect significantly body growth, plasma D‐glucose and insulin concentrations, pancreatic islet insulin content or the...

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Published inCell biochemistry and function Vol. 15; no. 4; pp. 287 - 291
Main Authors Ladriere, Laurence, Laghmich, Aouatif, Malaisse-Lagae, Francine, Malaisse, Willy J.
Format Journal Article
LanguageEnglish
Published Chichester, UK John Wiley & Sons, Ltd 01.12.1997
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Summary:Goto‐Kakizaki rats (GK rats) were given access for 4 weeks to a diet enriched with dehydroepiandrosterone (DHEA, 0·2 per cent, w/w). The incorporation of DHEA in the food failed to affect significantly body growth, plasma D‐glucose and insulin concentrations, pancreatic islet insulin content or the activity of both mitochondrial glycerophosphate dehydrogenase (mGDH) and NADP‐malate dehydrogenase (malic enzme) in islet homogenates. DHEA however, increased the activity of mGDH and, at least in male rates, that of the malic enzyme also in the liver. It lowered the abnormally high basal insulin release otherwise found in the islets from diabetic rats, and, as judged from the ratio of insulin output at 16·7 mM/2·8 mM D‐glucose, improved the cell responsiveness to the hexose. This coincided with a decreased plasma insulin/D‐glucose ratio, suggesting that the major effect of DHEA was to increase the sensitivity to insulin of extrapancreatic targets, thus resulting in a secondary improvement of cell secretory behaviour. © 1997 John Wiley & Sons, Ltd.
Bibliography:ark:/67375/WNG-42H1ZV5J-1
Belgian Foundation for Scientific Medical Research - No. 3.4513.94; No. 3.4542.96
istex:9134DEA87211FF6FEB5042E0CC85B349DCD38FD9
ArticleID:CBF753
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0263-6484
1099-0844
DOI:10.1002/(SICI)1099-0844(199712)15:4<287::AID-CBF753>3.0.CO;2-X