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SCAP/SREBP信号通路:肝脂肪变性的介导因子

The SCAP/SREBP Pathway: A Mediator of Hepatic Steatosis.

作者信息

Moon Young Ah

机构信息

Department of Molecular Medicine, Inha University School of Medicine, Incheon, Korea.

出版信息

Endocrinol Metab (Seoul). 2017 Mar;32(1):6-10. doi: 10.3803/EnM.2017.32.1.6. Epub 2017 Jan 19.

DOI:10.3803/EnM.2017.32.1.6
PMID:28116873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5368123/
Abstract

Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance, obesity, and dyslipidemia. NAFLD encompasses a wide range of states from the simple accumulation of triglycerides in the hepatocytes to serious states accompanied by inflammation and fibrosis in the liver. De novo lipogenesis has been shown to be a significant factor in the development of hepatic steatosis in insulin-resistant states. Sterol regulatory element binding protein-1c (SREBP-1c) is the main transcription factor that mediates the activation of lipogenesis, and SREBP cleavage activating protein (SCAP) is required for the activation of SREBPs. Here, recent animal studies that suggest SCAP as a therapeutic target for hepatic steatosis and hypertriglyceridemia are discussed.

摘要

非酒精性脂肪性肝病(NAFLD)与胰岛素抵抗、肥胖和血脂异常密切相关。NAFLD涵盖了从肝细胞内甘油三酯单纯积聚到伴有肝脏炎症和纤维化的严重状态等广泛的情况。在胰岛素抵抗状态下,从头脂肪生成已被证明是肝脂肪变性发展的一个重要因素。固醇调节元件结合蛋白-1c(SREBP-1c)是介导脂肪生成激活的主要转录因子,而SREBP裂解激活蛋白(SCAP)是SREBPs激活所必需的。在此,讨论了近期提示SCAP作为肝脂肪变性和高甘油三酯血症治疗靶点的动物研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa24/5368123/96b571dcb665/enm-32-6-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa24/5368123/c535038bf638/enm-32-6-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa24/5368123/96b571dcb665/enm-32-6-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa24/5368123/c535038bf638/enm-32-6-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa24/5368123/96b571dcb665/enm-32-6-g002.jpg

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