ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity - Archive ouverte HAL Access content directly
Journal Articles Cell Reports Year : 2022

ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity

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Fadila Benhamed
  • Function : Author
Anthony Emile
  • Function : Author
Sandrine Ellero-Simatos
  • Function : Author
  • PersonId : 1197485
Catherine Postic
  • Function : Author
Walter Wahli
  • Function : Author
  • PersonId : 1136620
Nicolas Loiseau
  • Function : Author

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.
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Dates and versions

hal-03695833 , version 1 (16-06-2022)

Licence

Attribution - CC BY 4.0

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Anne Fougerat, Gabriele Schoiswohl, Arnaud Polizzi, Marion Régnier, Carina Wagner, et al.. ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity. Cell Reports, 2022, 39 (10), ⟨10.1016/j.celrep.2022.110910⟩. ⟨hal-03695833⟩
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