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1
Insig: a significant integrator of nutrient and hormonal signals.Insig：营养和激素信号的重要整合因子。
J Clin Invest. 2004 Apr;113(8):1112-4. doi: 10.1172/JCI21450.
2
Molecular regulation of SREBP function: the Insig-SCAP connection and isoform-specific modulation of lipid synthesis.固醇调节元件结合蛋白（SREBP）功能的分子调控：胰岛素诱导基因（Insig）- 胆固醇调节元件结合蛋白裂解激活蛋白（SCAP）连接与脂质合成的亚型特异性调节
Biochem Cell Biol. 2004 Feb;82(1):201-11. doi: 10.1139/o03-090.
3
Overexpression of Insig-1 in the livers of transgenic mice inhibits SREBP processing and reduces insulin-stimulated lipogenesis.Insig-1在转基因小鼠肝脏中的过表达会抑制固醇调节元件结合蛋白（SREBP）的加工，并减少胰岛素刺激的脂肪生成。
J Clin Invest. 2004 Apr;113(8):1168-75. doi: 10.1172/JCI20978.
4
Role for sterol regulatory element-binding protein in activation of endothelial cells by phospholipid oxidation products.固醇调节元件结合蛋白在磷脂氧化产物激活内皮细胞中的作用。
Circ Res. 2004 Oct 15;95(8):780-8. doi: 10.1161/01.RES.0000146030.53089.18. Epub 2004 Sep 23.
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[Mechanism of action of sterol regulatory element binding proteins (SREBPs) in cholesterol and fatty-acid biosynthesis].[固醇调节元件结合蛋白（SREBPs）在胆固醇和脂肪酸生物合成中的作用机制]
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SREBP transcription factors: master regulators of lipid homeostasis.SREBP转录因子：脂质稳态的主要调节因子。
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CREating a SCAP-less liver keeps SREBPs pinned in the ER membrane and prevents increased lipid synthesis in response to low cholesterol and high insulin.构建无SCAP的肝脏可使固醇调节元件结合蛋白固定在内质网膜上，并防止因低胆固醇和高胰岛素而导致脂质合成增加。
Genes Dev. 2001 Aug 1;15(15):1873-8. doi: 10.1101/gad.916601.
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[Sterol regulatory element-binding proteins and lipid metabolism].[固醇调节元件结合蛋白与脂质代谢]
Sheng Li Ke Xue Jin Zhan. 2005 Jan;36(1):29-34.
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The SREBP pathway--insights from Insigs and insects.固醇调节元件结合蛋白（SREBP）途径——来自胰岛素诱导基因（Insigs）和昆虫的见解
Nat Rev Mol Cell Biol. 2003 Aug;4(8):631-40. doi: 10.1038/nrm1174.

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Effect of Cow-Calf Supplementation on Gene Expression, Processes, and Pathways Related to Adipogenesis and Lipogenesis in Muscle of F1 Angus × Nellore Cattle at Weaning.犊牛补饲对断奶时F1安格斯×内洛尔杂交肉牛肌肉中与脂肪生成和脂质生成相关的基因表达、过程及信号通路的影响
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Fatty acids homeostasis during fasting predicts protection from chemotherapy toxicity.禁食过程中脂肪酸的动态平衡可预测对化疗毒性的保护作用。
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The Diurnal Timing of Starvation Differently Impacts Murine Hepatic Gene Expression and Lipid Metabolism - A Systems Biology Analysis Using Self-Organizing Maps.饥饿的昼夜时间对小鼠肝脏基因表达和脂质代谢有不同影响——一项使用自组织映射的系统生物学分析
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FoxO1 Is Required for Most of the Metabolic and Hormonal Perturbations Produced by Hepatic Insulin Receptor Deletion in Male Mice.FoxO1 对于雄性小鼠肝脏胰岛素受体缺失引起的大多数代谢和激素紊乱都是必需的。
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Short-term arginine deprivation results in large-scale modulation of hepatic gene expression in both normal and tumor cells: microarray bioinformatic analysis.短期精氨酸剥夺导致正常细胞和肿瘤细胞中肝脏基因表达的大规模调节：微阵列生物信息学分析
Nutr Metab (Lond). 2006 Sep 8;3:37. doi: 10.1186/1743-7075-3-37.
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Insulin and glucose play a role in foam cell formation and function.胰岛素和葡萄糖在泡沫细胞的形成及功能方面发挥作用。
Cardiovasc Diabetol. 2006 Jun 20;5:13. doi: 10.1186/1475-2840-5-13.

本文引用的文献

1
Overexpression of Insig-1 in the livers of transgenic mice inhibits SREBP processing and reduces insulin-stimulated lipogenesis.Insig-1在转基因小鼠肝脏中的过表达会抑制固醇调节元件结合蛋白（SREBP）的加工，并减少胰岛素刺激的脂肪生成。
J Clin Invest. 2004 Apr;113(8):1168-75. doi: 10.1172/JCI20978.
2
Insulin-regulated hepatic gluconeogenesis through FOXO1-PGC-1alpha interaction.胰岛素通过FOXO1与PGC-1α的相互作用调节肝脏糖异生。
Nature. 2003 May 29;423(6939):550-5. doi: 10.1038/nature01667. Epub 2003 May 18.
3
Insig-2, a second endoplasmic reticulum protein that binds SCAP and blocks export of sterol regulatory element-binding proteins.Insig-2，一种与SCAP结合并阻止固醇调节元件结合蛋白输出的内质网蛋白。
Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):12753-8. doi: 10.1073/pnas.162488899. Epub 2002 Sep 19.
4
Crucial step in cholesterol homeostasis: sterols promote binding of SCAP to INSIG-1, a membrane protein that facilitates retention of SREBPs in ER.胆固醇稳态的关键步骤：固醇促进SCAP与INSIG-1结合，INSIG-1是一种膜蛋白，有助于将SREBPs保留在内质网中。
Cell. 2002 Aug 23;110(4):489-500. doi: 10.1016/s0092-8674(02)00872-3.
5
SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver.固醇调节元件结合蛋白：肝脏中胆固醇和脂肪酸合成完整程序的激活剂。
J Clin Invest. 2002 May;109(9):1125-31. doi: 10.1172/JCI15593.
6
Absence of sterol regulatory element-binding protein-1 (SREBP-1) ameliorates fatty livers but not obesity or insulin resistance in Lep(ob)/Lep(ob) mice.在瘦素缺乏（Lep(ob)/Lep(ob)）小鼠中，缺乏固醇调节元件结合蛋白-1（SREBP-1）可改善脂肪肝，但不能改善肥胖或胰岛素抵抗。
J Biol Chem. 2002 May 31;277(22):19353-7. doi: 10.1074/jbc.M201584200. Epub 2002 Mar 28.
7
Diminished hepatic response to fasting/refeeding and liver X receptor agonists in mice with selective deficiency of sterol regulatory element-binding protein-1c.固醇调节元件结合蛋白-1c选择性缺乏的小鼠对禁食/再进食及肝脏X受体激动剂的肝脏反应减弱。
J Biol Chem. 2002 Mar 15;277(11):9520-8. doi: 10.1074/jbc.M111421200. Epub 2002 Jan 8.
8
Increased expression of the sterol regulatory element-binding protein-1 gene in insulin receptor substrate-2(-/-) mouse liver.胰岛素受体底物-2基因敲除小鼠肝脏中固醇调节元件结合蛋白-1基因表达增加。
J Biol Chem. 2001 Oct 19;276(42):38337-40. doi: 10.1074/jbc.C100160200. Epub 2001 Aug 23.
9
Insulin inhibits transcription of IRS-2 gene in rat liver through an insulin response element (IRE) that resembles IREs of other insulin-repressed genes.胰岛素通过一个类似于其他胰岛素抑制基因的胰岛素反应元件（IRE）来抑制大鼠肝脏中IRS-2基因的转录。
Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):3756-61. doi: 10.1073/pnas.071054598. Epub 2001 Mar 20.
10
Regulation of mouse sterol regulatory element-binding protein-1c gene (SREBP-1c) by oxysterol receptors, LXRalpha and LXRbeta.氧甾醇受体LXRα和LXRβ对小鼠固醇调节元件结合蛋白-1c基因（SREBP-1c）的调控
Genes Dev. 2000 Nov 15;14(22):2819-30. doi: 10.1101/gad.844900.

Insig：营养和激素信号的重要整合因子。

Insig: a significant integrator of nutrient and hormonal signals.

作者信息

Attie Alan D

机构信息

Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.

出版信息

J Clin Invest. 2004 Apr;113(8):1112-4. doi: 10.1172/JCI21450.

DOI:10.1172/JCI21450
PMID:15085189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC385410/
Abstract

Lipogenesis is regulated by sterols and by insulin through the regulated expression and activation of the sterol regulatory element-binding proteins (SREBPs). A new study shows one way in which sterol and insulin regulation can be decoupled. In transgenic mice overexpressing a protein that regulates SREBP activation, lipogenesis is more sensitive to cholesterol and less sensitive to insulin.

摘要

脂肪生成受固醇类物质和胰岛素的调节，通过固醇调节元件结合蛋白（SREBPs）的表达调控和激活来实现。一项新研究揭示了一种能使固醇和胰岛素调节脱钩的方式。在过度表达一种调节SREBP激活蛋白的转基因小鼠中，脂肪生成对胆固醇更为敏感，而对胰岛素的敏感性降低。