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硫酸脱氢表雄酮(DHEAS)通过抑制 AMP 激活的蛋白激酶促进 MIN6 细胞胰岛素分泌。

Dehydroepiandrosterone-sulfate (DHEAS) promotes MIN6 cells insulin secretion via inhibition of AMP-activated protein kinase.

机构信息

Department of Metabolic and Endocrinology, Renji Hospital, Shanghai Jiaotong University School of Medicine, 160, Pujian Road, Pudong, Shanghai 200127, China.

出版信息

Biochem Biophys Res Commun. 2013 Nov 1;440(4):756-61. doi: 10.1016/j.bbrc.2013.10.002. Epub 2013 Oct 8.

Abstract

Derived from adrenal cortical, dehydroepiandrosterone-sulfate (DHEAS) is a precursor to androgens and estrogens, with various bioactivities. Although it has the property of anti-diabetes, the long-term effect of DHEAS on insulin secretion in beta-cells is still unclear. In this study, the effect of DHEAS on the insulin secretion activity in MIN6 cell lines in vitro was assessed. Insulin biosynthesis and secretion were stimulated by DHEAS for 24h. DHEAS inhibited the AMPK activation and upregulated the expression of ACC-1. These findings indicate that DHEAS may exert prominent stimulatory effects on insulin secretion partly via AMPK inhibition and ACC-1 upregulation.

摘要

来源于肾上腺皮质,硫酸脱氢表雄酮(DHEAS)是雄激素和雌激素的前体,具有多种生物活性。尽管它具有抗糖尿病的特性,但 DHEAS 对β细胞胰岛素分泌的长期影响尚不清楚。在这项研究中,评估了 DHEAS 对 MIN6 细胞系体外胰岛素分泌活性的影响。用 DHEAS 刺激胰岛素生物合成和分泌 24 小时。DHEAS 抑制 AMPK 的激活并上调 ACC-1 的表达。这些发现表明,DHEAS 可能通过抑制 AMPK 和上调 ACC-1 对胰岛素分泌产生显著的刺激作用。

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