G0S2

A small giant controller of lipolysis and adipose-liver fatty acid flux

Xiaodong Zhang, Bradlee L. Heckmann, Latoya E. Campbell, Jun D Liu

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The discovery of adipose triglyceride lipase (ATGL) and its coactivator comparative gene identification-58 (CGI-58) provided a major paradigm shift in the understanding of intracellular lipolysis in both adipocytes and nonadipocyte cells. The subsequent discovery of G0/G1 switch gene 2 (G0S2) as a potent endogenous inhibitor of ATGL revealed a unique mechanism governing lipolysis and fatty acid (FA) availability. G0S2 is highly conserved in vertebrates, and exhibits cyclical expression pattern between adipose tissue and liver that is critical to lipid flux and energy homeostasis in these two tissues. Biochemical and cell biological studies have demonstrated that a direct interaction with ATGL mediates G0S2's inhibitory effects on lipolysis and lipid droplet degradation. In this review we examine evidence obtained from recent in vitro and in vivo studies that lends support to the proof-of-principle concept that G0S2 functions as a master regulator of tissue-specific balance of TG storage vs. mobilization, partitioning of metabolic fuels between adipose and liver, and the whole-body adaptive energy response. This article is part of a Special Issue entitled: Recent Advances in Lipid Droplet Biology edited by Rosalind Coleman and Matthijs Hesselink.

Fingerprint

Switch Genes
Lipolysis
Lipase
Fatty Acids
Liver
Adipocytes
Vertebrates
Adipose Tissue
Homeostasis
Lipids
Genes
Lipid Droplets

Keywords

  • ATGL
  • Fatty acid
  • G0S2
  • Lipid droplet
  • Lipolysis
  • Triglyceride

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

G0S2 : A small giant controller of lipolysis and adipose-liver fatty acid flux. / Zhang, Xiaodong; Heckmann, Bradlee L.; Campbell, Latoya E.; Liu, Jun D.

In: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids, 2017.

Research output: Contribution to journalArticle

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