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

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.

• Authors: Ha-Jung Kim, Hong-Min Kim, Chu-Sook Kim, Choon-Soo Jeong, Hye-Sun Choi, Teruo Kawada, Byung-Sam Kim, Rina Yu
• Journal: FEBS letters (FEBS Lett) Vol. 585 Issue 14 Pg. 2285-90 (Jul 21 2011) ISSN: 1873-3468 [Electronic] England
• PMID: 21679708 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Chemical References

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

Topics

• Adipocytes (cytology, 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)