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Animals models of gastrointestinal and liver diseases. Animal models of alcohol-induced liver disease: pathophysiology, translational relevance, and challenges.胃肠道和肝脏疾病的动物模型。酒精性肝病的动物模型：发病机制、转化相关性和挑战。
Am J Physiol Gastrointest Liver Physiol. 2014 May 15;306(10):G819-23. doi: 10.1152/ajpgi.00041.2014. Epub 2014 Apr 3.
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Glucagon regulates gluconeogenesis through KAT2B- and WDR5-mediated epigenetic effects.胰高血糖素通过 KAT2B 和 WDR5 介导的表观遗传效应调节糖异生。
J Clin Invest. 2013 Oct;123(10):4318-28. doi: 10.1172/JCI69035. Epub 2013 Sep 24.
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Transcription factor ATF3 links host adaptive response to breast cancer metastasis.转录因子 ATF3 将宿主适应性反应与乳腺癌转移联系起来。
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PRMT5 modulates the metabolic response to fasting signals.PRMT5 调节对禁食信号的代谢反应。
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Binge ethanol and liver: new molecular developments. binge 乙醇与肝脏：新的分子进展。
Alcohol Clin Exp Res. 2013 Apr;37(4):550-7. doi: 10.1111/acer.12011. Epub 2013 Jan 24.
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Alcohol metabolism.酒精代谢。
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Cytochrome P4502E1, oxidative stress, JNK, and autophagy in acute alcohol-induced fatty liver.细胞色素 P4502E1、氧化应激、JNK 和自噬在急性酒精性脂肪肝中的作用。
Free Radic Biol Med. 2012 Sep 1;53(5):1170-80. doi: 10.1016/j.freeradbiomed.2012.06.029. Epub 2012 Jun 27.
8
Inositol-1,4,5-trisphosphate receptor regulates hepatic gluconeogenesis in fasting and diabetes.三磷酸肌醇受体调节禁食和糖尿病时的肝糖异生。
Nature. 2012 Apr 8;485(7396):128-32. doi: 10.1038/nature10988.
9
mTOR links incretin signaling to HIF induction in pancreatic beta cells.mTOR 通路将肠降血糖素信号传递到胰岛β细胞中的 HIF 诱导。
Proc Natl Acad Sci U S A. 2011 Oct 11;108(41):16876-82. doi: 10.1073/pnas.1114228108. Epub 2011 Sep 26.
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Hormonal regulation of hepatic glucose production in health and disease.激素对健康和疾病状态下肝脏葡萄糖生成的调节作用。
Cell Metab. 2011 Jul 6;14(1):9-19. doi: 10.1016/j.cmet.2011.06.003.

激活转录因子3（ATF3）介导乙醇对肝脏糖异生的抑制作用。

ATF3 mediates inhibitory effects of ethanol on hepatic gluconeogenesis.

作者信息

Tsai Wen-Wei, Matsumura Shigenobu, Liu Weiyi, Phillips Naomi G, Sonntag Tim, Hao Ergeng, Lee Soon, Hai Tsonwin, Montminy Marc

机构信息

Clayton Foundation Laboratories for Peptide Biology and.

Laboratory of Neuronal Structure and Function, The Salk Institute for Biological Studies, La Jolla, CA 92037; and.

出版信息

Proc Natl Acad Sci U S A. 2015 Mar 3;112(9):2699-704. doi: 10.1073/pnas.1424641112. Epub 2015 Feb 17.

DOI:10.1073/pnas.1424641112
PMID:25730876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4352786/
Abstract

Increases in circulating glucagon during fasting maintain glucose balance by stimulating hepatic gluconeogenesis. Acute ethanol intoxication promotes fasting hypoglycemia through an increase in hepatic NADH, which inhibits hepatic gluconeogenesis by reducing the conversion of lactate to pyruvate. Here we show that acute ethanol exposure also lowers fasting blood glucose concentrations by inhibiting the CREB-mediated activation of the gluconeogenic program in response to glucagon. Ethanol exposure blocked the recruitment of CREB and its coactivator CRTC2 to gluconeogenic promoters by up-regulating ATF3, a transcriptional repressor that also binds to cAMP-responsive elements and thereby down-regulates gluconeogenic genes. Targeted disruption of ATF3 decreased the effects of ethanol in fasted mice and in cultured hepatocytes. These results illustrate how the induction of transcription factors with overlapping specificity can lead to cross-coupling between stress and hormone-sensitive pathways.

摘要

禁食期间循环中胰高血糖素的增加通过刺激肝糖异生来维持葡萄糖平衡。急性乙醇中毒通过增加肝脏NADH促进禁食性低血糖，这通过减少乳酸向丙酮酸的转化来抑制肝糖异生。在此我们表明，急性乙醇暴露还通过抑制CREB介导的对胰高血糖素反应的糖异生程序激活来降低禁食血糖浓度。乙醇暴露通过上调ATF3来阻断CREB及其共激活因子CRTC2募集到糖异生启动子，ATF3是一种转录抑制因子，它也与cAMP反应元件结合，从而下调糖异生基因。靶向破坏ATF3可降低乙醇对禁食小鼠和培养肝细胞的影响。这些结果说明了具有重叠特异性的转录因子的诱导如何导致应激和激素敏感途径之间的交叉偶联。