Expression and significance of lipin1 and AMPKα in hepatic insulin resistance in diet-induced insulin resistance rats

Exp Clin Endocrinol Diabetes. 2012 Feb;120(2):84-8. doi: 10.1055/s-0031-1298013. Epub 2012 Jan 9.

Abstract

Background: Lipin1, a lately indentified adipokine, may link obesity with insulin resistance and diabetes. The present study aimed to investigate the changes and significance of lipin1 expression and lipin1-AMPK signaling in diet-induced hepatic insulin resistance.

Methods: 24 4-week-old Male Wistar rats were randomly divided into 2 groups: (1) control group (CO), (2) high-fat diet group (HF). Insulin sensitivity was evaluated by hyperinsulinemic-euglycemic clamp technique. The mRNA levels of α1 and α2 subunit of AMPKα as well as Lipin1 were measured using Real-time RT-PCR. The activities of AMPKα and Akt were evaluated by detection of p-AMPKα (Thr-172) and p-Akt (ser473) by Western blot.

Results: After treatment of 4 months, HF group showed significantly increased levels of body weight, fasting plasma glucose and insulin levels; Plasma and liver total cholesterol (TC), triglycerides (TG) levels were also markedly elevated; Lipin1 expression at both mRNA and protein levels were significantly deceased. Compared with CO group, the mRNA and protein levels of AMPKα1 and AMPKα2 were not changed, whereas the p-AMPK (Thr-172) and p-AKT (ser473) levels in liver were significantly decreased in HF group.

Conclusions: These findings indicated that the decrease in lipin1 expression and AMPKα activation may contribute to hepatic insulin resistance in diet-induced obese rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases / genetics*
  • AMP-Activated Protein Kinases / metabolism
  • AMP-Activated Protein Kinases / physiology
  • Animals
  • Diet
  • Disease Models, Animal
  • Gene Expression Regulation, Enzymologic / physiology
  • Insulin Resistance / genetics*
  • Lipid Metabolism / genetics
  • Lipids / blood
  • Liver / metabolism*
  • Liver / pathology
  • Male
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism
  • Nuclear Proteins / physiology
  • Obesity / etiology
  • Obesity / genetics
  • Obesity / metabolism
  • Obesity / pathology
  • Rats
  • Rats, Wistar

Substances

  • Lipids
  • Lpin1 protein, rat
  • Nuclear Proteins
  • AMP-Activated Protein Kinases
  • Prkaa1 protein, rat