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.
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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
期刊:
影响因子:
4.6
通讯作者:
Ren H
Ren H
中科院分区:
综合性期刊3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

文献摘要

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组织中的局部炎症是肥胖症代谢紊乱发展的主要原因之一。在某些组织中巨噬细胞的积聚可以诱导肥胖症的炎症反应。gpr 97在某些免疫细胞中高度表达,但其在炎症调节中的潜在作用尚未被清楚地揭示。在我们的研究中,我们研究了Gpr 97在调节高脂饮食(HFD)诱导的肥胖小鼠的巨噬细胞炎症和代谢功能障碍中的作用。Gpr 97基因敲除后,HFD喂养小鼠的主要代谢表型没有变化。与WT-HFD小鼠相比,在Gpr 97 −/−HFD小鼠的脂肪组织、肝脏和肾脏中观察到类似的病理学变化。在白色脂肪组织中,Gpr 97的缺失降低了M1-巨噬细胞的比率,增加了M2-巨噬细胞的比率,这与野生型HFD小鼠中观察到的相反。Gpr 97基因敲除后HFD小鼠肝、肾巨噬细胞浸润增多。此外,与野生型HFD小鼠相比,Gpr 97 −/−HFD小鼠肝脏和肾脏中的TNF-α水平更高。这些数据表明,Gpr 97可能是肥胖相关组织中局部炎症发展所需的,但在HFD诱导的肥胖中的代谢紊乱中不起作用。
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.