HVEM-deficient mice fed a high-fat diet are protected from adipose tissue inflammation and glucose intolerance
► We examined the effect of HVEM deficiency on obesity-induced inflammation and complications. ► HVEM-deficient mice or wild type mice were fed a high-fat diet (HFD). ► HFD-fed HVEM-deficient mice elicited a reduction in the number of macrophage/T cells infiltrated into adipose tissue. ► Proinflamma...
Saved in:
Published in | FEBS letters Vol. 585; no. 14; pp. 2285 - 2290 |
---|---|
Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier B.V
21.07.2011
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | ► We examined the effect of HVEM deficiency on obesity-induced inflammation and complications. ► HVEM-deficient mice or wild type mice were fed a high-fat diet (HFD). ► HFD-fed HVEM-deficient mice elicited a reduction in the number of macrophage/T cells infiltrated into adipose tissue. ► Proinflammatory cytokine levels were also decreased in the adipose tissue of HFD-fed HVEM. ► Glucose intolerance and insulin sensitivity were markedly improved in the HFD-fed HVEM-deficient mice.
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. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0014-5793 1873-3468 |
DOI: | 10.1016/j.febslet.2011.05.057 |