Phosphorylation events implicating p38 and PI3K mediate tungstate-effects in MIN6 beta cells

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• 作者：S ; ra Piquer ; Sí ; lvia Barceló ; -Batllori ; Marta Julià ; Nuria Marzo ; Belen Nadal ; Joan J. Guinovart ; Ramon Gomis
• 关键词：Tungstate ; Beta cell ; Insulin secretion ; Pancreatic duodenal homeobox-1 ; p38 MAP kinase ; Phosphatidylinositol 3-kinase
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2007
• 出版时间：29 June 2007
• 年：2007
• 卷：358
• 期：2
• 页码：385-391
• 全文大小：428 K

文摘

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.