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• W3041832574 endingPage "118073" @default.
• W3041832574 startingPage "118073" @default.
• W3041832574 abstract "The preservation of pancreatic beta-cell function is crucial for the treatment of type 2 diabetes. Inhibition of class I histone deacetylase (HDAC) has been proved to protect beta-cells from palmitate- or cytokine-induced apoptosis and increase insulin secretion. However, the underlying molecular mechanism is unclear. Rat islets were isolated for insulin secretion, real-time PCR, RNA- sequencing, ChIP-PCR, and oxygen consumption rate analysis after treated with the HDAC1 and HDAC3 inhibitor MS-275. MS-275 pretreatment significantly potentiated insulin secretion from rat islets. RNA-sequencing revealed that multiple signaling pathways were involved in MS-275-regulated islet function. Cacna1g and Adcy1 in calcium and cAMP signaling pathways were up-regulated in MS-275-treated islets, which was validated by real-time PCR. The expressions of the two genes displayed a similar increase in islets isolated from mice treated with MS-275. Knockdown of HDAC1 elevated Cacna1g and Adcy1 expressions in islets. ChIP-sequencing analysis showed that the pan-HDAC inhibitor sodium butyrate increased H3K27 acetylation level in the upstream region of Adcy1 and the promoter region of Cacna1g. ChIP-PCR revealed a similar result in MS-275-treated rat islets. However, MS-275 had minor effect on glucose-induced oxygen consumption rate in rat islets. Unlike glucose, MS-275 did not alter the expressions of glucose-sensitive genes such as Glut2 and Gck, but elevated intracellular Ca2+ concentration in beta-cells. Our findings support the notion that MS-275-potentiated insulin secretion is involved in calcium and cAMP signaling-mediated gene expressions independent of glucose oxidation. Therefore, HDAC inhibition may serve as a therapeutic strategy for type 2 diabetes." @default.
• W3041832574 created "2020-07-16" @default.
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• W3041832574 date "2020-09-01" @default.
• W3041832574 modified "2023-09-27" @default.
• W3041832574 title "Histone deacetylase inhibition by MS-275 potentiates glucose-stimulated insulin secretion without affecting glucose oxidation" @default.
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• W3041832574 doi "https://doi.org/10.1016/j.lfs.2020.118073" @default.
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