Forced Hepatic Overexpression of CEACAM1 Curtails Diet-Induced Insulin Resistance

Diabetes. 2015 Aug;64(8):2780-90. doi: 10.2337/db14-1772. Epub 2015 May 13.

Abstract

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) regulates insulin sensitivity by promoting hepatic insulin clearance. Liver-specific inactivation or global null-mutation of Ceacam1 impairs hepatic insulin extraction to cause chronic hyperinsulinemia, resulting in insulin resistance and visceral obesity. In this study we investigated whether diet-induced insulin resistance implicates changes in hepatic CEACAM1. We report that feeding C57/BL6J mice a high-fat diet reduced hepatic CEACAM1 levels by >50% beginning at 21 days, causing hyperinsulinemia, insulin resistance, and elevation in hepatic triacylglycerol content. Conversely, liver-specific inducible CEACAM1 expression prevented hyperinsulinemia and markedly limited insulin resistance and hepatic lipid accumulation that were induced by prolonged high-fat intake. This was partly mediated by increased hepatic β-fatty acid oxidation and energy expenditure. The data demonstrate that the high-fat diet reduced hepatic CEACAM1 expression and that overexpressing CEACAM1 in liver curtailed diet-induced metabolic abnormalities by protecting hepatic insulin clearance.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Antigens, CD / genetics
  • Antigens, CD / metabolism*
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism*
  • Diet, High-Fat*
  • Energy Metabolism / physiology
  • Fatty Acids / metabolism
  • Hyperinsulinism / genetics
  • Hyperinsulinism / metabolism
  • Insulin / blood
  • Insulin Resistance / genetics*
  • Liver / metabolism*
  • Mice
  • Mice, Transgenic

Substances

  • Antigens, CD
  • CD66 antigens
  • Cell Adhesion Molecules
  • Fatty Acids
  • Insulin