ATGL Promotes Autophagy/Lipophagy via SIRT1 to Control Hepatic Lipid Droplet Catabolism

Aishwarya Sathyanarayan, Mara T Mashek, Douglas Mashek

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189 Scopus citations


Hepatic lipid droplet (LD) catabolism is thought to occur via cytosolic lipases such as adipose triglyceride lipase (ATGL) or through autophagy of LDs, a process known as lipophagy. We tested the potential interplay between these metabolic processes and its effects on hepatic lipid metabolism. We show that hepatic ATGL is both necessary and sufficient to induce both autophagy and lipophagy. Moreover, lipophagy is required for ATGL to promote LD catabolism and the subsequent oxidation of hydrolyzed fatty acids (FAs). Following previous work showing that ATGL promotes sirtuin 1 (SIRT1) activity, studies in liver-specific SIRT1−/− mice and in primary hepatocytes reveal that SIRT1 is required for ATGL-mediated induction of autophagy and lipophagy. Taken together, these studies show that ATGL-mediated signaling via SIRT1 promotes autophagy/lipophagy as a primary means to control hepatic LD catabolism and FA oxidation.

Original languageEnglish (US)
Pages (from-to)1-9
Number of pages9
JournalCell reports
Issue number1
StatePublished - Apr 4 2017

Bibliographical note

Funding Information:
This work was supported by grants from the NIH (DK090364) to D.G.M. and the Minnesota Obesity Center (NIH DK050456). The authors express their gratitude to Charles Najt for his expertise with LD isolations, as well as Codruta Vizoli and Mary McCourt for their excellent technical support. They also extend their gratitude to the staff at the University of Minnesota's Imaging Center, in particular, Grant Barthel and Alexander Cramer.

Publisher Copyright:
© 2017 The Author(s)


  • ATGL
  • SIRT1
  • autophagy
  • fatty acid oxidation
  • lipid droplets
  • lipolysis
  • lipophagy
  • liver metabolism


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