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ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity

2022; Cell Press; Volume: 39; Issue: 10 Linguagem: Inglês

10.1016/j.celrep.2022.110910

2639-1856

Anne Fougerat, Gabriele Schoiswohl, Arnaud Polizzi, Marion Régnier, Carina Wagner, Sarra Smati, Tiffany Fougeray, Yannick Lippi, Frédèric Lasserre, Ilyès Raho, Valentine Melin, Blandine Tramunt, Raphaël Métivier, Caroline Sommer, Fadila Benhamed, Chantal Alkhoury, Franziska Greulich, Céline Jouffe, Anthony Emile, Michael Schupp, Pierre Gourdy, Patricia Dubot, Thierry Levade, Delphine Meynard, Sandrine Ellero‐Simatos, Laurence Gamet‐Payrastre, Ganna Panasyuk, N. Henriette Uhlenhaut, Ez‐Zoubir Amri, Céline Cruciani‐Guglielmacci, Catherine Postic, Walter Wahli, Nicolas Loiseau, Alexandra Montagner, Dominique Langin, Achim Lass, Hervé Guillou,

Lipid metabolism and biosynthesis

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 β