| Literature DB >> 35675775 |
Anne Fougerat1, Gabriele Schoiswohl2, Arnaud Polizzi1, Marion Régnier1, Carina Wagner3, Sarra Smati4, Tiffany Fougeray1, Yannick Lippi1, Frederic Lasserre1, Ilyès Raho5, Valentine Melin1, Blandine Tramunt6, Raphaël Métivier7, Caroline Sommer1, Fadila Benhamed8, Chantal Alkhoury9, Franziska Greulich10, Céline Jouffe11, Anthony Emile1, Michael Schupp12, Pierre Gourdy6, Patricia Dubot13, Thierry Levade13, Delphine Meynard14, Sandrine Ellero-Simatos1, Laurence Gamet-Payrastre1, Ganna Panasyuk9, Henriette Uhlenhaut15, Ez-Zoubir Amri16, Céline Cruciani-Guglielmacci5, Catherine Postic8, Walter Wahli17, Nicolas Loiseau1, Alexandra Montagner18, Dominique Langin19, Achim Lass20, Hervé Guillou21.
Abstract
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.Entities:
Keywords: ATGL; CP: Metabolism; FGF21; PPARα; fasting; ketogenesis; lipolysis
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Year: 2022 PMID： 35675775 DOI： 10.1016/j.celrep.2022.110910
Source DB: PubMed Journal: Cell Rep Impact factor: 9.995