Acarbose treatment or islet transplantation increase FAD-glycerophosphate dehydrogenase content in islets of diabetic rats

Citation
Me. Fabregat et al., Acarbose treatment or islet transplantation increase FAD-glycerophosphate dehydrogenase content in islets of diabetic rats, MED SCI RES, 27(6), 1999, pp. 393-396
Citations number
20
Categorie Soggetti
Medical Research General Topics
Journal title
MEDICAL SCIENCE RESEARCH
ISSN journal
02698951 → ACNP
Volume
27
Issue
6
Year of publication
1999
Pages
393 - 396
Database
ISI
SICI code
0269-8951(199906)27:6<393:ATOITI>2.0.ZU;2-T
Abstract
Male adult rats injected with streptozotocin during the neonatal period (ST Z rats) showed low body weight, high fluid intake, increased glycaemia, low plasma insulin concentration, decreased islet content in FAD-glycerophosph ate dehydrogenase (mGDH), low activity of mGDH in islet homogenates, low is let insulin content and decreased secretory responsiveness of the islets to D-glucose, as compared to control animals of same sex and age. When the ST Z rats were given access to acarbose (40 mg/100 g of food) for one month, t he fluid intake, glycaemia, pancreatic islet content in mGDH and activity o f this enzyme in islet homogenates were all improved, but the plasma insuli n concentration remained unchanged. Likewise, when the STZ rats were grafte d with 1,000-1,200 islets from normal rats, the mGDH content of pancreatic islets again increased. This now coincided with a significant increase in p lasma insulin concentration, but a somewhat lower increment (Delta) in insu lin output, in response to a rise in D-glucose concentration from 2.8 to 16 .7 mmol/l, in the islets from transplanted rats (Delta = 21.4 +/- 6.2 mu U/ islet per 90 min) than in those from untreated STZ rats (Delta = 39.5 +/- 8 .8 mu U/islet per 90 min). By comparison with data obtained in other experi mental models of B-cell dysfunction, these findings suggest that sustained hyperglycaemia unfavourably affects expression of the mGDH gene in pancreat ic islets of animals suffering from a primary alteration of their insulin-s ecreting cell population. Med Sci Res 27:393-396 (C) 1999 Lippincott Willia ms & Wilkins.