CMKLR1 deficiency influences glucose tolerance and thermogenesis in mice on high fat diet
CMKLR1 deficiency influences glucose tolerance and thermogenesis in mice on high fat diet
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CMKLR1 缺陷影响高脂饮食小鼠的葡萄糖耐量和生热作用
DOI：
10.1016/j.bbrc.2016.03.026
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发表时间：
2016-04-29
影响因子：
3.1
通讯作者：
Zhang, Jian V.
中科院分区：
文献类型：
--
作者：
Huang, Chen;Wang, Miaomiao;Zhang, Jian V.
肥胖已成为一种全球性流行病，导致2型糖尿病患病率增加。CMKLR1是趋化因子受体之一，在先天免疫和适应性免疫、炎症、代谢和生殖等生理和病理活动中具有广泛的功能。在我们的研究中，CMKLR1缺乏并不影响体重的增加，但会加剧葡萄糖耐受不良，增加血清胰岛素水平，并促进高脂饮食小鼠的胰岛素抵抗。CMKLR1基因敲除（KO）小鼠在正常和寒冷环境中产热相关基因的表达均降低，表明CMKLR1影响了小鼠的产热过程。冷暴露诱导野生型HFD小鼠体重显著下降，并改善葡萄糖耐量和胰岛素抵抗，但对CMKLR 11（0）HFD小鼠无明显影响。在体外实验中，CMKLR1的缺失并没有显著影响脂肪组织来源的基质血管成纤维细胞（SVFs）的分化，但抑制了产热相关基因的表达。总的来说，这些数据表明，CMKLR1缺乏诱导葡萄糖代谢的不平衡，并损害高饮食模型中的冷诱导产热过程。(C)2016由Elsevier Inc.出版
Obesity has become a global epidemic disease, contributing to increases in the prevalence of type 2 diabetes. CMKLR1, one of the receptors for chemerin, has a wide range of functions in physiological and pathological activity, including innate and adaptive immunity, inflammation, metabolism and reproduction. In our study, CMKLR1 deficiency did not influence the gain of body weight but did exacerbate glucose intolerance, increase serum insulin level, and promote insulin resistance in mice on high fat diets. The expression of thermogenesis related genes was examined and indicated to decrease in CMKLR1 knockout (KO) mice in both normal and cold environments, which indicated CMKLR1 influence the thermogenesis process. Cold exposure induced significant body mass decrease and improved glucose tolerance and insulin resistance in wild type HFD mice but had no obvious effect on CMKLR1 1(0 HFD mice. In vitro, loss of CMKLR1 did not significantly influence the differentiation of stromal vascular fibroblasts (SVFs) derived from adipose tissue, but did suppress the expression of thermogenesis related genes. Collectively, these data demonstrate that CMKLR1 deficiency induces inbalance of glucose metabolism and impairs the cold induced-thermogenesis process in high diet models. (C) 2016 Published by Elsevier Inc.