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 in | Cell biochemistry and function Vol. 15; no. 4; pp. 287 - 291 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Chichester, UK
John Wiley & Sons, Ltd
01.12.1997
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Subjects | |
Online Access | Get full text |
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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. |
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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 |