Gpr97 is dispensable for metabolic syndrome but is involved in macrophage inflammation in high-fat diet-induced obesity in mice.
Gpr97 is dispensable for metabolic syndrome but is involved in macrophage inflammation in high-fat diet-induced obesity in mice.
复制标题
Gpr97对于代谢综合征来说是可有可无的,但与高脂饮食诱导的小鼠肥胖症中的巨噬细胞炎症有关
DOI:
10.1038/srep24649
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发表时间:
2016-04-19
影响因子:
4.6
通讯作者:
Ren H
中科院分区:
文献类型:
--
作者:
Shi J;Zhang X;Wang S;Wang J;Du B;Wang Z;Liu M;Jiang W;Qian M;Ren H
Local inflammation in tissues is one of primary causes in development of metabolic disorder in obesity. The accumulation of macrophages in some tissues can induce inflammatory reactions in obesity. Gpr97 is highly expressed in some immunocytes, but its potential role in inflammatory regulation has not been revealed clearly. In our research, we investigated Gpr97 in regulating macrophage inflammation and metabolic dysfunction in the high-fat diet (HFD)-induced obese mice. The major metabolic phenotyping were not different afterGpr97knockout in HFD-fed mice. Similar pathological alterations in adipose tissue, liver and kidney were observed inGpr97−/−HFD mice compared with WT-HFD mice. In white adipose tissue, loss of Gpr97 reduced the ratio of M1-macrophages and increased the M2-macrophage ratio, which was opposite to that seen in the wild-type HFD mice. More macrophages invaded in the liver and kidney after Gpr97 knockout in HFD mice. Furthermore, the levels of TNF-α were higher in the liver and kidney ofGpr97−/−HFD mice compared to those in wild-type HFD mice. The data indicate that Gpr97 might be required for local inflammation development in obesity-relative tissues, but does not play a role in metabolic disorder in HFD-induced obesity.