amp的k-胰岛素信号通路.pdf

Cell Metabolism Article AMPK Phosphorylates and Inhibits SREBP Activity to Attenuate Hepatic Steatosis and Atherosclerosis in Diet-Induced Insulin-Resistant Mice Yu Li,1 Shanqin Xu,1 Maria M. Mihaylova,2,3 Bin Zheng,4 Xiuyun Hou,1 Bingbing Jiang,1 Ogyi Park,5 Zhijun Luo,1 Etienne Lefai,6 John Y.-J. Shyy,7 Bin Gao,5 Michel Wierzbicki,8 Tony J. Verbeuren,8 Reuben J. Shaw,2,3 Richard A. Cohen,1 and Mengwei Zang1,* 1Department of Medicine, Vascular Biology Section, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02481, USA 2Howard Hughes Medical Institute 3Molecular and Cell Biology Laboratory The Salk Institute for Biological Studies, La Jolla, CA 92037, USA 4Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA 5Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA 6Lyon University, INSERM U1060, INRA U1235, CarMeN Laboratory, University Lyon-1, F- 69600 Oullins, France 7Division of Biomedical Sciences, University of California, Riverside, Riverside, CA 92093, USA 8Institut de Recherche Servier, 92150 Suresnes, France *Correspondence: mwzang1@bu.edu DOI 10.1016/j.cmet.2011.03.009 SUMMARY (SREBP) is a key lipogenic transcription factor that is nutritionally regulated by glucose and insulin (Horton et al., 2002; Goldstein AMPK has emerged as a critical mechanism for and Brown, 2008). SREBP-1c preferentially regulates the lipogenic salutary effects of polyphenols on lipid metabolic process by act