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Fougerat, A.* ; Schoiswohl, G.* ; Polizzi, A.* ; Régnier, M.* ; Wagner, C.* ; Smati, S.* ; Fougeray, T.* ; Lippi, Y.* ; Lasserre, F.* ; Raho, I.* ; Melin, V.* ; Tramunt, B.* ; Métivier, R.* ; Sommer, C.* ; Benhamed, F.* ; Alkhoury, C.* ; Greulich, F.* ; Jouffe, C. ; Emile, A.* ; Schupp, M.* ; Gourdy, P.* ; Dubot, P.* ; Levade, T.* ; Meynard, D.* ; Ellero-Simatos, S.* ; Gamet-Payrastre, L.* ; Panasyuk, G.* ; Uhlenhaut, N.H. ; Amri, E.Z.* ; Cruciani-Guglielmacci, C.* ; Postic, C.* ; Wahli, W.* ; Loiseau, N.* ; Montagner, A.* ; Langin, D.* ; Lass, A.* ; Guillou, H.*

ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity.

Cell Rep. 39:110910 (2022)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
In hepatocytes, peroxisome proliferator-activated receptor α (PPARα) orchestrates a genomic and metabolic response required for homeostasis during fasting. This includes the biosynthesis of ketone bodies and of fibroblast growth factor 21 (FGF21). Here we show that in the absence of adipose triglyceride lipase (ATGL) in adipocytes, ketone body and FGF21 production is impaired upon fasting. Liver gene expression analysis highlights a set of fasting-induced genes sensitive to both ATGL deletion in adipocytes and PPARα deletion in hepatocytes. Adipose tissue lipolysis induced by activation of the β3-adrenergic receptor also triggers such PPARα-dependent responses not only in the liver but also in brown adipose tissue (BAT). Intact PPARα activity in hepatocytes is required for the cross-talk between adipose tissues and the liver during fat mobilization.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Atgl ; Cp: Metabolism ; Fgf21 ; Pparα ; Fasting ; Ketogenesis ; Lipolysis
Language english
Publication Year 2022
HGF-reported in Year 2022
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Journal Cell Reports
Quellenangaben Volume: 39, Issue: 10, Pages: , Article Number: 110910 Supplement: ,
Publisher Cell Press
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes and Cancer (IDC)
POF-Topic(s) 30201 - Metabolic Health
90000 - German Center for Diabetes Research
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502594-001
G-501900-227
DOI 10.1016/j.celrep.2022.110910
WOS ID WOS:000819468000002
PubMed ID 35675775
Erfassungsdatum 2022-07-11
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