期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 116, 期 50, 页码 25250-25259出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1911189116
关键词
alcohol; circadian; acetylation; liver; metabolism
资金
- University of California, Irvine, Hitachi-Nomura fund
- Japan Society for the Promotion of Science
- National Cancer Institute of the US NIH [NIH T32 2T32CA009054-36A1]
- European Research Council (ERC MSCA-IF-2016 MetEpiClock) [749869]
- INSERM, NIH
- Pilot Project Program of the National Institute on Alcohol Abuse and Alcoholism-funded Southern California Research Center for ALPD and Cirrhosis [P50AA011999]
- Defense Advanced Research Projects Agency [D17AP00002]
- NIH [GM123558]
- Marie Curie Actions (MSCA) [749869] Funding Source: Marie Curie Actions (MSCA)
Binge drinking and chronic exposure to ethanol contribute to alcoholic liver diseases (ALDs). A potential link between ALDs and circadian disruption has been observed, though how different patterns of alcohol consumption differentially impact hepatic circadian metabolism remains virtually unexplored. Using acute versus chronic ethanol feeding, we reveal differential reprogramming of the circadian transcriptome in the liver. Specifically, rewiring of diurnal SREBP transcriptional pathway leads to distinct hepatic signatures in acetyl-CoA metabolism that are translated into the subcellular patterns of protein acetylation. Thus, distinct drinking patterns of alcohol dictate differential adaptation of hepatic circadian metabolism.
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