Oral selenate improves glucose homeostasis and partly reverses abnormal expression of liver glycolytic and gluconeogenic enzymes in diabetic rats


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Becker D., Reul B., ÖZÇELİKAY A. T., Buchet J., Henquin J., Brichard S.

DIABETOLOGIA, cilt.39, sa.1, ss.3-11, 1996 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 39 Sayı: 1
  • Basım Tarihi: 1996
  • Doi Numarası: 10.1007/bf00400407
  • Dergi Adı: DIABETOLOGIA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.3-11
  • Anahtar Kelimeler: selenium, glycolytic enzymes, gluconeogenic enzymes, gene expression, streptozotocin-diabetic rats, ATOMIC-ABSORPTION SPECTROMETRY, VANADATE TREATMENT, MESSENGER-RNA, MOLECULAR-CLONING, PYRUVATE-KINASE, BLOOD-GLUCOSE, SELENIUM, INSULIN, METABOLISM, PROTEIN
  • Ankara Üniversitesi Adresli: Evet

Özet

Selenium is a trace element that exerts certain insulin-like actions in vitro. In this study, we evaluated its in vivo effects on the glucose homeostasis of rats made diabetic and insulin-deficient by streptozotocin. Na2SeO4 was administered ad libitum in drinking water and/or food for 10 weeks. The elevated plasma glucose levels (similar to 25 mmol/l) and glucosuria (similar to 85 mmol/day) of untreated rats were decreased by 50 and 80 %, respectively, by selenate treatment. The beneficial effect of selenate was also evident during oral and intravenous glucose tolerance tests: the integrated glucose responses were decreased by 40-50 % as compared to those in untreated rats. These effects were not due to an increase in plasma insulin levels, Compared to non-diabetic rats, pancreatic insulin reserves were reduced by more than 90 % in treated and untreated diabetic rats. The hepatic activities and mRNA levels of two key glycolytic enzymes, glucokinase and L-type pyruvate kinase were blunted in diabetic rats. They increased similar to two- to threefold after selenate treatment, to reach 40-75 % of the values in non-diabetic rats. In contrast, elevated activity and mRNA levels of the gluconeogenic enzyme, phosphoenolpyruvate carboxykinase, were reduced by 40-65 % after selenate administration. Since selenate induced a moderate decrease in body weight due to an anorexigenic effect, we checked that there was no improvement of glucose homeostasis or hepatic glucose metabolism in an additional group of calorie-restricted diabetic rats, which was weight-matched with the selenate group. In addition, no obvious toxic side-effects on the kidney or liver were observed in the rats receiving selenate. In conclusion, selenate induces a sustained improvement of glucose homeostasis in streptozotocin-diabetic rats by an insulin-like action, which involves partial correction of altered pretranslational regulatory mechanisms in liver metabolism.