期刊
OBESITY
卷 22, 期 5, 页码 1264-1274出版社
WILEY
DOI: 10.1002/oby.20642
关键词
-
资金
- NRSA [F32-DK083903]
- National Center for Advancing Translational Sciences [8KL2TR000112-05]
- [RO-1-ES017290]
- [R21-DK088522]
Objective: Chemokine (C-X-C motif) receptor 3 (CXCR3) is a chemokine receptor involved in the regulation of immune cell trafficking and activation. Increased CXCR3 expression in the visceral adipose of obese humans and mice was observed. A pathophysiologic role for CXCR3 in diet-induced obesity (DIO) was hypothesized. Methods: Wild-type (WT) C57B/L6J and chemokine receptor 3 knockout (CXCR3(-/-)) mice were fed a high-fat diet (HFD) for 20 weeks followed by assessment of glucose metabolism and visceral adipose tissue (VAT) inflammation. Results: CXCR3(-/-) mice exhibited lower fasting glucose and improved glucose tolerance compared with WT-HFD mice, despite similar body mass. HFD-induced VAT innate and adaptive immune cell infiltration, including immature myeloid cells (CD11b(+) F4/80(Io) Ly6C(+)), were markedly ameliorated in CXCR3(-/-) mice. In vitro IBIDI and in vivo migration assays demonstrated no CXCR3- mediated effect on macrophage or monocyte migration, respectively. CXCR3(-/-) macrophages, however, had a blunted response to interferon-gamma, a T(H)1 cytokine that induces macrophage activation. Conclusions: A previously unreported role for CXCR3 in the development of HFD-induced insulin resistance (IR) and VAT macrophage infiltration in mice was demonstrated. Our results support pharmaceutical targeting of the CXCR3 receptor as a potential treatment for obesity/IR.
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