Effect of dehydroepiandrosterone in hereditarily diabetic rats

✍ Scribed by Laurence Ladriere; Aouatif Laghmich; Francine Malaisse-Lagae; Willy J. Malaisse

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 106 KB
• Volume: 15
• Category: Article
• ISSN: 0263-6484
• DOI: 10.1002/(sici)1099-0844(199712)15:4<287::aid-cbf753>3.0.co;2-x

✦ Synopsis

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 aect signi®cantly 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 eect of DHEA was to increase the sensitivity to insulin of extrapancreatic targets, thus resulting in a secondary improvement of cell secretory behaviour.