HVEM-deficient mice fed a high-fat diet are protected from adipose tissue inflammation and glucose intolerance

FEBS Lett. 2011 Jul 21;585(14):2285-90. doi: 10.1016/j.febslet.2011.05.057. Epub 2011 Jun 12.

Abstract

HVEM is a member of the TNF receptor superfamily that plays a role in the development of various inflammatory diseases. In this study, we show that HVEM deficiency attenuates adipose tissue inflammatory responses and glucose intolerance in diet-induced obesity. Feeding a high-fat diet (HFD) to HVEM-deficient mice elicited a reduction in the number of macrophages and T cells infiltrated into adipose tissue. Proinflammatory cytokine levels in the adipose tissue decreased in HFD-fed HVEM-deficient mice, while levels of the anti-inflammatory cytokine IL-10 increased. Moreover, glucose intolerance and insulin sensitivity were markedly improved in the HFD-fed HVEM-deficient mice. These findings indicate that HVEM may be a useful target for combating obesity-induced inflammatory responses and insulin resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / metabolism
  • Adipose Tissue / physiopathology*
  • Animals
  • Blood Glucose / metabolism
  • Cytokines / metabolism
  • Dietary Fats / pharmacology*
  • Glucose Intolerance*
  • Inflammation / physiopathology*
  • Insulin / metabolism
  • Insulin Resistance / physiology
  • Mice
  • Obesity / physiopathology
  • Receptors, Tumor Necrosis Factor, Member 14 / deficiency*

Substances

  • Blood Glucose
  • Cytokines
  • Dietary Fats
  • Insulin
  • Receptors, Tumor Necrosis Factor, Member 14
  • Tnfrsf14 protein, mouse