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Interferon‐gamma Induced Adipose Inflammation Linked to the Impairment of Vascular Function in Type 2 diabetic mice
Author(s) -
Zhang Hanrui,
Zhang Cuihua
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb536
Subject(s) - medicine , endocrinology , adipose tissue , inflammation , mesenteric arteries , sodium nitroprusside , adipocyte , nitric oxide , artery
We hypothesized that IFNγ induces inflammatory cell infiltration and chemoattractant gene expression in mesenteric adipose tissue (MAT) and impairs vascular function of mesenteric arteries (MA) of type 2 diabetic mice. Acetylcholine (ACh)‐induced vasodilation was impaired in Lepr db vs. m Lepr db , but sodium nitroprusside (SNP)‐induced vasodilation was comparable. Both anti‐IFNγ and anti‐MCP‐1 improved endothelial function in Lepr db , while IFNγ induced impaired vascular function in m Lepr db . Mesenteric bed weight and MAT adipocyte size were greatly elevated (P<0.05) in Lepr db vs. m Lepr db . Immunohistochemical staining results revealed that CD3‐positve T‐lymphocytes, Mac‐3 positive macrophages infiltration into the adventitia of small mesenteric arteries was significantly increased in Lepr db and IFNγ‐treated m Lepr db , suggesting the possible crosstalk between adipose inflammation and vascular dysfunction. Western blotting results showed that anti‐IFNγ decreased MAT IFNγ and MCP‐1 protein expression in Lepr db ,while IFNγ and MCP‐1 expression was elevated in IFNγ‐treated m Lepr db . Anti‐MCP‐1 treatment only decreased MCP‐1 expression in Lepr db without affecting IFNγ levels, indicating that IFNγ may act as an initiator of MAT inflammation. These results suggest a role for IFNγ in the regulation of visceral adipose inflammatory response and vascular dysfunction in type 2 diabetes.