Ablation of a galectin preferentially expressed in adipocytes increases lipolysis, reduces adiposity, and improves insulin sensitivity in mice

Ri Yao Yang, Lan Yu, James L. Graham, Daniel K. Hsu, Kevin C K Lloyd, Peter J Havel, Fu-Tong Liu

Research output: Contribution to journalArticle

35 Scopus citations

Abstract

The breakdown of triglycerides, or lipolysis, is a tightly controlled process that regulates fat mobilization in accord with an animal's energy needs. It is well established that lipolysis is stimulated by hormones that signal energy demand and is suppressed by the antilipolytic hormoneinsulin.However,much still remains to be learned about regulation of lipolysis by intracellular signaling pathways in adipocytes. Here we show that galectin-12, a member of a β-galactoside-binding lectin family preferentially expressed by adipocytes, functions as an intrinsic negative regulator of lipolysis. Galectin-12 is primarily localized on lipid droplets and regulates lipolytic protein kinase A signaling by acting upstream of phosphodiesterase activity to control cAMP levels. Ablation of galectin-12 in mice results in increased adipocyte mitochondrial respiration, reduced adiposity, and ameliorated insulin resistance/glucose intolerance. This study identifies unique properties of this intracellular galectin that is localized to an organelle and performs a critical function in lipid metabolism. These findings add to the significant functions exhibited by intracellular galectins, and have important therapeutic implications for human metabolic disorders.

Original languageEnglish (US)
Pages (from-to)18696-18701
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume108
Issue number46
DOIs
StatePublished - Nov 15 2011

Keywords

  • Diabetes
  • Energy metabolism
  • Obesity

ASJC Scopus subject areas

  • General

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