A Novel Function of Hepatic FOG2 in Insulin Sensitivity and Lipid Metabolism Through PPARα

Diabetes. 2016 Aug;65(8):2151-63. doi: 10.2337/db15-1565. Epub 2016 May 3.

Abstract

Friend of GATA 2 (FOG2) is a transcriptional cofactor involved mostly in cardiac function. The aim of this study was to investigate the role of hepatic FOG2 in insulin sensitivity and lipid accumulation. FOG2 overexpression by adenovirus-expressing FOG2 (Ad-FOG2) significantly attenuates insulin signaling in hepatocytes in vitro. Opposite effects were observed when FOG2 was knocked down through adenovirus-expressing small hairpin RNA for FOG2 (Ad-shFOG2). Furthermore, FOG2 knockdown by Ad-shFOG2 ameliorated insulin resistance in leptin receptor-mutated (db/db) mice, and FOG2 overexpression by Ad-FOG2 attenuated insulin sensitivity in C57BL/6J wild-type (WT) mice. In addition, Ad-FOG2 reduced, whereas Ad-shFOG2 promoted, hepatic triglyceride (TG) accumulation in WT mice under fed or fasted conditions, which was associated with increased or decreased hepatic peroxisome proliferator-activated receptor α (PPARα) expression, respectively. Moreover, the improved insulin sensitivity and increased hepatic TG accumulation by Ad-shFOG2 were largely reversed by adenovirus-expressing PPARα (Ad-PPARα) in WT mice. Finally, we generated FOG2 liver-specific knockout mice and found that they exhibit enhanced insulin sensitivity and elevated hepatic TG accumulation, which were also reversed by Ad-PPARα. Taken together, the results demonstrate a novel function of hepatic FOG2 in insulin sensitivity and lipid metabolism through PPARα.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / metabolism
  • Cholesterol / metabolism
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Fatty Acids, Nonesterified / metabolism
  • Female
  • Glucose Tolerance Test
  • Glycogen / metabolism
  • Insulin / metabolism
  • Insulin Resistance / genetics*
  • Lipid Metabolism / genetics*
  • Liver / metabolism*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • PPAR alpha / genetics
  • PPAR alpha / metabolism*
  • Receptors, Leptin / genetics
  • Receptors, Leptin / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Triglycerides / metabolism

Substances

  • Blood Glucose
  • DNA-Binding Proteins
  • Fatty Acids, Nonesterified
  • Insulin
  • PPAR alpha
  • Receptors, Leptin
  • Transcription Factors
  • Triglycerides
  • Zfpm2 protein, mouse
  • Glycogen
  • Cholesterol