Abstract
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 after Gpr97 knockout in HFD-fed mice. Similar pathological alterations in adipose tissue, liver, and kidney were observed in Gpr97−/− 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 of Gpr97−/− 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.
Highlights
Receptors (GPCRs) have been identified as important regulators in obese metabolic disorder, such as GPR119 and GPR12015,16
high-fat diet (HFD)-fed mice were significantly heavier than chow-fed mice, especially after 12-weeks (P < 0.05), no alteration was shown in Gpr97-deficient HFD-fed mice (Fig. 1b)
According to the alteration in the mRNA level of the macrophage marker F4/80, we found that Gpr[97] deficiency can cause a reduction in macrophage invasion of White adipose tissue (WAT) in HFD-fed mice (Fig. 3b)
Summary
Receptors (GPCRs) have been identified as important regulators in obese metabolic disorder, such as GPR119 and GPR12015,16. It was reported that the expression of GPR97 was significantly down-regulated when using colony-stimulating factor-1 (CSF-1/M-CSF) or granulocyte macrophage colony-stimulating factor (GM-CSF) to stimulate primary human macrophages differentiation from monocytes[21], but its molecular mechanism in macrophage polarization and the related inflammatory response have not yet been reported. It seems that GPR97 might play an important role in immune system, but whether it functions in inflammation during obesity has yet to be determined. We used Gpr97-knockout mice to elucidate whether Gpr[97] has a role in macrophage-related inflammation and obesity-induced metabolic syndrome
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