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本文引用的文献

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A circadian rhythm orchestrated by histone deacetylase 3 controls hepatic lipid metabolism.组蛋白去乙酰化酶 3 调控的生物钟节律控制肝脏脂质代谢。
Science. 2011 Mar 11;331(6022):1315-9. doi: 10.1126/science.1198125.
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Detecting and quantitating physiological endoplasmic reticulum stress.检测和定量生理性内质网应激。
Methods Enzymol. 2011;490:137-46. doi: 10.1016/B978-0-12-385114-7.00008-8.
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The binary switch that controls the life and death decisions of ER stressed β cells.控制内质网应激 β 细胞生死决策的二进制开关。
Curr Opin Cell Biol. 2011 Apr;23(2):207-15. doi: 10.1016/j.ceb.2010.11.005. Epub 2010 Dec 16.
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Angptl4 protects against severe proinflammatory effects of saturated fat by inhibiting fatty acid uptake into mesenteric lymph node macrophages.Angptl4 通过抑制脂肪酸摄取到肠系膜淋巴结巨噬细胞中来防止饱和脂肪的严重促炎作用。
Cell Metab. 2010 Dec 1;12(6):580-92. doi: 10.1016/j.cmet.2010.11.002.
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Emerging roles for XBP1, a sUPeR transcription factor.XBP1的新作用,一种超级转录因子。
Gene Expr. 2010;15(1):13-25. doi: 10.3727/105221610x12819686555051.
6
Regulation of unfolded protein response modulator XBP1s by acetylation and deacetylation.未折叠蛋白反应调节剂 XBP1s 的乙酰化和去乙酰化调节。
Biochem J. 2011 Jan 1;433(1):245-52. doi: 10.1042/BJ20101293.
7
Toll-like receptors: linking inflammation to metabolism. toll 样受体:将炎症与代谢联系起来。
Trends Endocrinol Metab. 2011 Jan;22(1):16-23. doi: 10.1016/j.tem.2010.08.007. Epub 2010 Oct 1.
8
A Phos-tag-based approach reveals the extent of physiological endoplasmic reticulum stress.基于 Phos-tag 的方法揭示了生理内质网应激的程度。
PLoS One. 2010 Jul 16;5(7):e11621. doi: 10.1371/journal.pone.0011621.
9
XBP-1 couples endoplasmic reticulum stress to augmented IFN-beta induction via a cis-acting enhancer in macrophages.XBP-1 通过巨噬细胞中的顺式作用增强子将内质网应激与增强的 IFN-β诱导偶联。
J Immunol. 2010 Aug 15;185(4):2324-30. doi: 10.4049/jimmunol.0903052. Epub 2010 Jul 21.
10
Defective hepatic autophagy in obesity promotes ER stress and causes insulin resistance.肥胖导致的肝脏自噬缺陷会促进内质网应激,并引起胰岛素抵抗。
Cell Metab. 2010 Jun 9;11(6):467-78. doi: 10.1016/j.cmet.2010.04.005.

压力与肥胖:IRE1α-XBP1 在代谢紊乱中的作用。

Stressed out about obesity: IRE1α-XBP1 in metabolic disorders.

机构信息

Division of Nutritional Sciences, Cornell University, Ithaca, NY, USA.

出版信息

Trends Endocrinol Metab. 2011 Sep;22(9):374-81. doi: 10.1016/j.tem.2011.05.002. Epub 2011 Jun 22.

DOI:10.1016/j.tem.2011.05.002
PMID:21703863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3163776/
Abstract

The global obesity epidemic is associated with a series of health-threatening diseases including type 2 diabetes. Accumulating evidence suggest that the physiology and homeostasis of the endoplasmic reticulum (ER) is intimately involved in the underlying mechanisms linking obesity and diabetes. Specifically, recent studies indicate a crucial role for the inositol-requiring enzyme 1α (IRE1α)/X-box binding protein 1 (XBP1) pathway, the most conserved branch of the unfolded protein response (UPR), in glucose and lipid metabolism as well as in insulin function. Focusing on the IRE1α-XBP1 pathway, we review recent advances in our understanding of the role of UPR in obesity and obesity-associated metabolic disorders.

摘要

全球肥胖症流行与一系列威胁健康的疾病相关,包括 2 型糖尿病。越来越多的证据表明,内质网(ER)的生理学和内稳态与肥胖和糖尿病之间的潜在机制密切相关。具体而言,最近的研究表明,需要肌醇的酶 1α(IRE1α)/X 盒结合蛋白 1(XBP1)途径,即未折叠蛋白反应(UPR)中最保守的分支,在葡萄糖和脂质代谢以及胰岛素功能中起着关键作用。本文聚焦于 IRE1α-XBP1 途径,综述了我们对 UPR 在肥胖和肥胖相关代谢紊乱中的作用的最新认识。