Phosphorylation events implicating p38 and PI3K mediate tungstate-effects in MIN6 beta cells
- Endocrinology and Diabetes Unit, Department of Medicine, Hospital Clinic/IDIBAPS, University of Barcelona, Barcelona (Spain)
- Department of Biochemistry and Molecular Biology and IRB-Barcelona Science Park, University of Barcelona (Spain)
Oral administration of sodium tungstate is an effective treatment for diabetes in animal models. Several lines of evidence indicate the pancreatic beta cell as one of the targets of tungstate action. Here, we examined the molecular mechanism by which this compound exerts its effects on the beta cell line MIN6. Tungstate treatment induced phosphorylation and subsequent activation of p38 and PI3K which in turn are implicated in tungstate PDX-1 nuclear localization and activation. Although no effect was observed in glucose-induced insulin secretion we found that tungstate activates basal insulin release, a process driven, at least in part, by activation of p38. These results show a direct involvement of p38 and PI3K phosphorylation in the mechanism of action of tungstate in the beta cell.
- OSTI ID:
- 20991402
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 358, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2007.04.143; PII: S0006-291X(07)00823-6; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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