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- W2101391555 abstract "Resveratrol, a polyphenol compound, is known for its effects on energy homeostasis. With properties of energy sensors mediating effects of calorie restriction, sirtuins are targets of resveratrol. The mammalian sirtuin homolog SIRT1 is a protein deacetylase playing a role in glucose metabolism and islet function. Here, we investigated the effects of resveratrol and possible link with SIRT1 in β-cells. Insulinoma INS-1E cells and human islets were cultured with resveratrol before analyzing their physiological responses. Treatment of INS-1E cells for 24 h with 25 μm resveratrol resulted in marked potentiation of glucose-stimulated insulin secretion. This effect was associated with elevated glycolytic flux, resulting in increased glucose oxidation, ATP generation, and mitochondrial oxygen consumption. Such changes correlated with up-regulation of key genes for β-cell function, i.e. Glut2, glucokinase, Pdx-1, Hnf-1α, and Tfam. In human islets, chronic resveratrol treatment similarly increased both the glucose secretory response and expression of the same set of genes, eventually restoring the glucose response in islets obtained from one type 2 diabetic donor. Overexpression of Sirt1 in INS-1E cells potentiated resveratrol effects on insulin secretion. Conversely, inhibition of SIRT1 achieved either by expression of an inactive mutant or by using the EX-527 inhibitor, both abolished resveratrol effects on glucose responses. Treatment of INS-1E cells with EX-527 also prevented resveratrol-induced up-regulation of Glut2, glucokinase, Pdx-1, and Tfam. Resveratrol markedly enhanced the glucose response of INS-1E cells and human islets, even after removal of the compound from the medium. These effects were mediated by and fully dependent on active SIRT1, defining a new role for SIRT1 in the regulation of insulin secretion. Resveratrol, a polyphenol compound, is known for its effects on energy homeostasis. With properties of energy sensors mediating effects of calorie restriction, sirtuins are targets of resveratrol. The mammalian sirtuin homolog SIRT1 is a protein deacetylase playing a role in glucose metabolism and islet function. Here, we investigated the effects of resveratrol and possible link with SIRT1 in β-cells. Insulinoma INS-1E cells and human islets were cultured with resveratrol before analyzing their physiological responses. Treatment of INS-1E cells for 24 h with 25 μm resveratrol resulted in marked potentiation of glucose-stimulated insulin secretion. This effect was associated with elevated glycolytic flux, resulting in increased glucose oxidation, ATP generation, and mitochondrial oxygen consumption. Such changes correlated with up-regulation of key genes for β-cell function, i.e. Glut2, glucokinase, Pdx-1, Hnf-1α, and Tfam. In human islets, chronic resveratrol treatment similarly increased both the glucose secretory response and expression of the same set of genes, eventually restoring the glucose response in islets obtained from one type 2 diabetic donor. Overexpression of Sirt1 in INS-1E cells potentiated resveratrol effects on insulin secretion. Conversely, inhibition of SIRT1 achieved either by expression of an inactive mutant or by using the EX-527 inhibitor, both abolished resveratrol effects on glucose responses. Treatment of INS-1E cells with EX-527 also prevented resveratrol-induced up-regulation of Glut2, glucokinase, Pdx-1, and Tfam. Resveratrol markedly enhanced the glucose response of INS-1E cells and human islets, even after removal of the compound from the medium. These effects were mediated by and fully dependent on active SIRT1, defining a new role for SIRT1 in the regulation of insulin secretion." @default.
- W2101391555 created "2016-06-24" @default.
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- W2101391555 date "2011-02-01" @default.
- W2101391555 modified "2023-10-09" @default.
- W2101391555 title "Resveratrol Potentiates Glucose-stimulated Insulin Secretion in INS-1E β-Cells and Human Islets through a SIRT1-dependent Mechanism" @default.
- W2101391555 cites W1562122315 @default.
- W2101391555 cites W1913661755 @default.
- W2101391555 cites W1951075546 @default.
- W2101391555 cites W1969408132 @default.
- W2101391555 cites W1973163466 @default.
- W2101391555 cites W1973378704 @default.
- W2101391555 cites W1979754659 @default.
- W2101391555 cites W1985308585 @default.
- W2101391555 cites W1986399270 @default.
- W2101391555 cites W1992375025 @default.
- W2101391555 cites W1992678387 @default.
- W2101391555 cites W1995095187 @default.
- W2101391555 cites W1997145913 @default.
- W2101391555 cites W2005789183 @default.
- W2101391555 cites W2007842741 @default.
- W2101391555 cites W2013841882 @default.
- W2101391555 cites W2026145411 @default.
- W2101391555 cites W2031149113 @default.
- W2101391555 cites W2031372661 @default.
- W2101391555 cites W2038353863 @default.
- W2101391555 cites W2038818919 @default.
- W2101391555 cites W2041959419 @default.
- W2101391555 cites W2042710774 @default.
- W2101391555 cites W2044578262 @default.
- W2101391555 cites W2050776635 @default.
- W2101391555 cites W2053827043 @default.
- W2101391555 cites W2056673958 @default.
- W2101391555 cites W2059267070 @default.
- W2101391555 cites W2060457885 @default.
- W2101391555 cites W2061113221 @default.
- W2101391555 cites W2066253340 @default.
- W2101391555 cites W2067754307 @default.
- W2101391555 cites W2069752613 @default.
- W2101391555 cites W2074740541 @default.
- W2101391555 cites W2077722171 @default.
- W2101391555 cites W2078023359 @default.
- W2101391555 cites W2080057943 @default.
- W2101391555 cites W2083434423 @default.
- W2101391555 cites W2088381487 @default.
- W2101391555 cites W2089165207 @default.
- W2101391555 cites W2089560759 @default.
- W2101391555 cites W2091412980 @default.
- W2101391555 cites W2096361448 @default.
- W2101391555 cites W2103416697 @default.
- W2101391555 cites W2104595034 @default.
- W2101391555 cites W2106073742 @default.
- W2101391555 cites W2111831728 @default.
- W2101391555 cites W2116979396 @default.
- W2101391555 cites W2119976307 @default.
- W2101391555 cites W2125121177 @default.
- W2101391555 cites W2127594986 @default.
- W2101391555 cites W2130185420 @default.
- W2101391555 cites W2134294998 @default.
- W2101391555 cites W2140751228 @default.
- W2101391555 cites W2143687302 @default.
- W2101391555 cites W2144600435 @default.
- W2101391555 cites W2145101949 @default.
- W2101391555 cites W2147081499 @default.
- W2101391555 cites W2147788578 @default.
- W2101391555 cites W2149703257 @default.
- W2101391555 cites W2152101492 @default.
- W2101391555 cites W2156158875 @default.
- W2101391555 cites W2157649587 @default.
- W2101391555 cites W2167226448 @default.
- W2101391555 cites W2168180935 @default.
- W2101391555 doi "https://doi.org/10.1074/jbc.m110.176842" @default.
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- W2101391555 hasPublicationYear "2011" @default.
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