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June 7, 2022
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info:eu-repo/semantics/altIdentifier/doi/10.1016/j.celrep.2022.110910
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info:eu-repo/semantics/altIdentifier/pmid/35675775
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info:eu-repo/semantics/altIdentifier/eissn/2211-1247
This document is linked to :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_8E8213483E108
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
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Fat tissue Body fat tissues Adipose tissue Fatty tissueCite this document
A. Fougerat et al., « ATGL-dependent white adipose tissue lipolysis controls hepatocyte PPARα activity. », Serveur académique Lausannois, ID : 10.1016/j.celrep.2022.110910
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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 β 3 -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.
