TY - JOUR
T1 - Distinct metabolic adaptation of liver circadian pathways to acute and chronic patterns of alcohol intake
AU - Gaucher, Jonathan
AU - Kinouchi, Kenichiro
AU - Ceglia, Nicholas
AU - Montellier, Emilie
AU - Peleg, Shahaf
AU - Greco, Carolina Magdalen
AU - Schmidt, Andreas
AU - Forne, Ignasi
AU - Masri, Selma
AU - Baldi, Pierre
AU - Imhof, Axel
AU - Sassone-Corsi, Paolo
N1 - Funding Information:
ACKNOWLEDGMENTS. We thank all members of the P.S.-C. laboratory for stimulating discussion and technical assistance. We also thank Dr. Tsukamoto (University of Southern California) for insight and support. We also thank Melanie Oakes, Seung-Ah Chung, and Yuzo Kanomata at the Genomics High-Throughput Facility at the University of California, Irvine. J.G. was supported by a postdoctoral fellowship from the University of California, Irvine, Hitachi-Nomura fund. K.K. was supported by a postdoctoral fellowship from the Japan Society for the Promotion of Science. C.M.G. was supported by the National Cancer Institute of the US NIH (NIH T32 2T32CA009054-36A1) and by European Research Council (ERC MSCA-IF-2016 MetEpiClock 749869). Work in the P.S.-C. laboratory was supported by INSERM, NIH, in part by the Pilot Project Program of the National Institute on Alcohol Abuse and Alcoholism-funded Southern California Research Center for ALPD and Cirrhosis (P50AA011999). Work by N.C. and P.B. was in part supported by Defense Advanced Research Projects Agency grant D17AP00002 and NIH grant GM123558 to P.B. These authors would also like to acknowledge computing support by Yuzo Kanomata.
Funding Information:
We thank all members of the P.S.-C. laboratory for stimulating discussion and technical assistance. We also thank Dr. Tsukamoto (University of Southern California) for insight and support. We also thank Melanie Oakes, Seung-Ah Chung, and Yuzo Kanomata at the Genomics High-Throughput Facility at the University of California, Irvine. J.G. was supported by a postdoctoral fellowship from the University of California, Irvine, Hitachi-Nomura fund. K.K. was supported by a postdoctoral fellowship from the Japan Society for the Promotion of Science. C.M.G. was supported by the National Cancer Institute of the US NIH (NIH T32 2T32CA009054-36A1) and by European Research Council (ERC MSCA-IF-2016 MetEpiClock 749869). Work in the P.S.-C. laboratorywas supported by INSERM, NIH, in part by the Pilot Project Program of the National Institute on Alcohol Abuse and Alcoholism-funded Southern California Research Center for ALPD and Cirrhosis (P50AA011999). Work by N.C. and P.B. was in part supported by Defense Advanced Research Projects Agency grant D17AP00002 and NIH grant GM123558 to P.B. These authors would also like to acknowledge computing support by Yuzo Kanomata.*%blankline%*
Publisher Copyright:
© 2019 National Academy of Sciences. All rights reserved.
PY - 2019/12/10
Y1 - 2019/12/10
N2 - 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.
AB - 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.
KW - Acetylation
KW - Alcohol
KW - Circadian
KW - Liver
KW - Metabolism
UR - http://www.scopus.com/inward/record.url?scp=85076375384&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85076375384&partnerID=8YFLogxK
U2 - 10.1073/pnas.1911189116
DO - 10.1073/pnas.1911189116
M3 - Article
C2 - 31757851
AN - SCOPUS:85076375384
SN - 0027-8424
VL - 116
SP - 25250
EP - 25259
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 50
ER -