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Gpr97 is dispensable for metabolic syndrome but is involved in macrophage inflammation in high-fat diet-induced obesity in mice.

Shi J, Zhang X, Wang S, Wang J, Du B, Wang Z, Liu M, Jiang W, Qian M, Ren H - Sci Rep (2016)

Bottom Line: Gpr97 is highly expressed in some immunocytes, but its potential role in inflammatory regulation has not been revealed clearly.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.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.

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.

No MeSH data available.


Related in: MedlinePlus

Analysis of metabolite, transcriptional, inflammatory factors in mRNA levels in the livers of HFD-fed mice.The expression of genes in mRNA levels which are associated with transcriptional regulators (a), mitochondrially encoded genes (b), fatty acid oxidation, hepatic mitochondrial function, lipogenesis, glucose metabolism (c) and inflammatory factors (d) in HFD mice. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 0.01 < P < 0.05.
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f5: Analysis of metabolite, transcriptional, inflammatory factors in mRNA levels in the livers of HFD-fed mice.The expression of genes in mRNA levels which are associated with transcriptional regulators (a), mitochondrially encoded genes (b), fatty acid oxidation, hepatic mitochondrial function, lipogenesis, glucose metabolism (c) and inflammatory factors (d) in HFD mice. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 0.01 < P < 0.05.

Mentions: To determine the function of Gpr97 in the liver of HFD mice, we measured the mRNA expression of metabolic factors, including those involved in transcriptional regulators which influence pathways of fatty acid oxidation (FoxO1, Pparα, Pgc1α, Pgc1β, Errα, Prc and Atp5s) (Fig. 5a), mitochondrially encoded genes (ND1, ND2, ND4, ATP6, ATP8 and COX2) (Fig. 5b), fatty acid oxidation (Acox1, Fgf21), mitochondrial function (Cs, Atp5g1), lipogenesis (SREBP2, Fasn), glucose metabolism (PEPCK, G6Pase) (Fig. 5c), and inflammation (F4/80, CD68, TNF-α, IL-6 and IL-1β) (Fig. 5d) 25. These genes, which are involved in the major metabolic pathways and inflammatory reactions in the liver, showed slightly higher expression in Gpr97−/− mice than in WT mice under a HFD-fed. Gpr97 deficiency, therefore, will aggravate some key gene expression which are involved in hepatic metabolism such as transcriptional regulation in fatty acid oxidation and mitochondrial function. Moreover, the inflammatory factor TNF-α, IL-6 and IL-1β were increased after Gpr97 knockout in HFD-fed mice. The higher expression of F4/80 and CD68 indicates that more macrophages gathered in the liver of Gpr97−/− HFD mice, and that the loss of Gpr97 may cause more serious inflammation and metabolic stress in the liver of obese mice.


Gpr97 is dispensable for metabolic syndrome but is involved in macrophage inflammation in high-fat diet-induced obesity in mice.

Shi J, Zhang X, Wang S, Wang J, Du B, Wang Z, Liu M, Jiang W, Qian M, Ren H - Sci Rep (2016)

Analysis of metabolite, transcriptional, inflammatory factors in mRNA levels in the livers of HFD-fed mice.The expression of genes in mRNA levels which are associated with transcriptional regulators (a), mitochondrially encoded genes (b), fatty acid oxidation, hepatic mitochondrial function, lipogenesis, glucose metabolism (c) and inflammatory factors (d) in HFD mice. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 0.01 < P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4835759&req=5

f5: Analysis of metabolite, transcriptional, inflammatory factors in mRNA levels in the livers of HFD-fed mice.The expression of genes in mRNA levels which are associated with transcriptional regulators (a), mitochondrially encoded genes (b), fatty acid oxidation, hepatic mitochondrial function, lipogenesis, glucose metabolism (c) and inflammatory factors (d) in HFD mice. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 0.01 < P < 0.05.
Mentions: To determine the function of Gpr97 in the liver of HFD mice, we measured the mRNA expression of metabolic factors, including those involved in transcriptional regulators which influence pathways of fatty acid oxidation (FoxO1, Pparα, Pgc1α, Pgc1β, Errα, Prc and Atp5s) (Fig. 5a), mitochondrially encoded genes (ND1, ND2, ND4, ATP6, ATP8 and COX2) (Fig. 5b), fatty acid oxidation (Acox1, Fgf21), mitochondrial function (Cs, Atp5g1), lipogenesis (SREBP2, Fasn), glucose metabolism (PEPCK, G6Pase) (Fig. 5c), and inflammation (F4/80, CD68, TNF-α, IL-6 and IL-1β) (Fig. 5d) 25. These genes, which are involved in the major metabolic pathways and inflammatory reactions in the liver, showed slightly higher expression in Gpr97−/− mice than in WT mice under a HFD-fed. Gpr97 deficiency, therefore, will aggravate some key gene expression which are involved in hepatic metabolism such as transcriptional regulation in fatty acid oxidation and mitochondrial function. Moreover, the inflammatory factor TNF-α, IL-6 and IL-1β were increased after Gpr97 knockout in HFD-fed mice. The higher expression of F4/80 and CD68 indicates that more macrophages gathered in the liver of Gpr97−/− HFD mice, and that the loss of Gpr97 may cause more serious inflammation and metabolic stress in the liver of obese mice.

Bottom Line: Gpr97 is highly expressed in some immunocytes, but its potential role in inflammatory regulation has not been revealed clearly.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.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.

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.

No MeSH data available.


Related in: MedlinePlus