Activation by vanadate of glycolysis in hepatocytes from diabetic rats

Juan Enrique Rodriguez Gil, Maria Fatima Bosch Tubert, Anna M. Gómez-Foix, Cristina Fillat, Joan J. Guinovart

Research output: Contribution to journalArticleResearchpeer-review

18 Citations (Scopus)

Abstract

In hepatocytes from starved streptozocin-induced diabetic rats, vanadate increases the glycolytic flux because it raises the levels of fructose-2,6-bisphosphate (Fru-2,6-P2), the main regulatory metabolite of this pathway. This effect of vanadate on Fru-2,6-P2levels is time and dose dependent, and it remains in cells incubated in a calcium-depleted medium. Vanadate is also able to counteract the decrease on Fru-2,6-P2levels produced by glucagon, colforsin, or exogenous cAMP. However, vanadate does not modify 6-phosphofructo-2-kinase and pyruvate kinase activities, but it does counteract the inactivation of these enzymes induced by glucagon. Likewise, Fru-2,6-P2ase activity is also not affected by vanadate. In addition, vanadate is able to increase the production of both lactate and CO2in hepatocytes from streptozocin-induced diabetic rats incubated in the presence of glucose in the medium. Vanadate behaves as a glycolytic effector in these cells, and this effect may be related to its ability to normalize blood glucose levels in diabetic animals.
Original languageEnglish
Pages (from-to)1355-1359
JournalDiabetes
Volume40
Issue number10
DOIs
Publication statusPublished - 1 Feb 1991

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