Regulation of hepatokine gene expression in response to fasting and feeding: Influence of PPAR-α and insulin-dependent signalling in hepatocytes

Diabetes Metab. 2020 Apr;46(2):129-136. doi: 10.1016/j.diabet.2019.05.005. Epub 2019 Jun 1.

Abstract

Aim: In hepatocytes, the peroxisome proliferator-activated receptor (PPAR)-α and insulin receptor (IR) are critical for transcriptional responses to fasting and feeding, respectively. The present report analyzes the effects of nutritional status (fasting vs feeding) on the expression of a large panel of hepatokines in hepatocyte-specific PPAR-α (Pparαhep-/-) and IR (IRhep-/-) null mice.

Methods: Pparαhep-/- and IRhep-/- mice, and their wild-type littermates, were subjected to fasting or feeding metabolic challenges, then analyzed for hepatokine gene expression. Experiments were conducted in mice of both genders.

Results: Our data confirmed that PPAR-α is essential for regulating fasting-induced Fgf21 and Angptl4 expression. In mice lacking PPAR-α, fasting led to increased Igfbp1 and Gdf15 gene expression. In the absence of hepatic IR, feeding induced overexpression of Igfbp1, follistatin (Fst) and adropin (Enho), and reduced activin E (Inhbe) expression. Gender had only a modest influence on hepatokine gene expression in the liver.

Conclusion: The present results highlight the potential roles of hepatokines as a class of hormones that substantially influence nutritional regulation in both female and male mice.

Keywords: Hepatokines; Insulin receptor; Nutritional regulation; PPAR-α.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiopoietin-Like Protein 4 / genetics
  • Angiopoietin-Like Protein 4 / metabolism
  • Animals
  • Eating / physiology*
  • Fasting / metabolism*
  • Fibroblast Growth Factors / genetics
  • Fibroblast Growth Factors / metabolism
  • Gene Expression
  • Hepatocytes / metabolism*
  • Insulin / metabolism
  • Mice
  • Mice, Knockout
  • PPAR alpha / genetics
  • PPAR alpha / metabolism*
  • Receptor, Insulin / genetics
  • Receptor, Insulin / metabolism*
  • Signal Transduction / physiology*

Substances

  • Angiopoietin-Like Protein 4
  • Insulin
  • PPAR alpha
  • fibroblast growth factor 21
  • Fibroblast Growth Factors
  • Receptor, Insulin