Abstract
Phosphatidylinositol 3-kinase (PI3-kinase) has been implicated in the regulation of vesicular transport. We examined the roles of PI3-kinase in the glucose-induced insulin secretion from the pancreatic beta cell line MIN6 by using wortmannin, a potent inhibitor of PI3-kinase. Low concentrations of wortmannin markedly potentiated the glucose-induced insulin secretion. This effect was probably mediated by PI3-kinase inhibition. Furthermore, wortmannin completely canceled the suppressive effect of insulin-like growth factor-I on insulin secretion from MIN6 cells. On the basis of these results, we discuss a possible role of PI3-kinase in the negative feed-back regulation of insulin secretion.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Androstadienes / metabolism
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Androstadienes / pharmacology
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Cell Line
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Insulin / metabolism*
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Insulin Secretion
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Insulin-Like Growth Factor I / pharmacology
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Islets of Langerhans / enzymology
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Islets of Langerhans / metabolism*
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Phosphatidylinositol 3-Kinases
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Phosphotransferases (Alcohol Group Acceptor) / antagonists & inhibitors
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Phosphotransferases (Alcohol Group Acceptor) / metabolism*
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Protein Binding
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Proteins / metabolism
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Somatostatin / pharmacology
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Wortmannin
Substances
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Androstadienes
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Insulin
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Proteins
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Somatostatin
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Insulin-Like Growth Factor I
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Phosphatidylinositol 3-Kinases
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Phosphotransferases (Alcohol Group Acceptor)
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Wortmannin