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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

The obese phenotype and fasting blood glucose of high-fat diet (HFD)-induced mice.(a) Food intake. The average grams food intake in WT and Gpr97−/− mice each month. (n = 8) (b) Body weight. The growth of body weight in WT and Gpr97−/− mice by chow or HFD feeding. (n = 6–8) (c) Intraperitoneal glucose tolerance test (ipGTT). The levels of blood glucose were detected at 0, 15, 30, 45 and 60 minutes after intraperitoneal inject in chow or HFD fed mice (n = 8). Data are shown as means ± s.e.m. **0.01 < P < 0.05, ***P < 0.01.
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f1: The obese phenotype and fasting blood glucose of high-fat diet (HFD)-induced mice.(a) Food intake. The average grams food intake in WT and Gpr97−/− mice each month. (n = 8) (b) Body weight. The growth of body weight in WT and Gpr97−/− mice by chow or HFD feeding. (n = 6–8) (c) Intraperitoneal glucose tolerance test (ipGTT). The levels of blood glucose were detected at 0, 15, 30, 45 and 60 minutes after intraperitoneal inject in chow or HFD fed mice (n = 8). Data are shown as means ± s.e.m. **0.01 < P < 0.05, ***P < 0.01.

Mentions: The mice were fed with 60% calories in fat for 16 weeks to induce the metabolic syndrome. Metabolic phenotype, including food intake, body weight and glucose tolerance, was examined in mice. The quantity of food intake and body weight was recorded once a month. According to the collected data, there was no obvious difference in food intake between WT and Gpr97−/− HFD-fed mice (Fig. 1a). Although 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). Moreover, we used an intraperitoneal glucose tolerance test (ipGTT) to examine glucose tolerance in our mice model. The fasting blood glucose of HFD mice was much higher than that of the chow-fed mice from 15 min (P < 0.01), but there was no change after loss of Gpr97 in HFD mice compared with WT HFD mice (Fig. 1c). These data indicate that Gpr97 deficiency does not influence the body weight or glucose tolerance of HFD 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)

The obese phenotype and fasting blood glucose of high-fat diet (HFD)-induced mice.(a) Food intake. The average grams food intake in WT and Gpr97−/− mice each month. (n = 8) (b) Body weight. The growth of body weight in WT and Gpr97−/− mice by chow or HFD feeding. (n = 6–8) (c) Intraperitoneal glucose tolerance test (ipGTT). The levels of blood glucose were detected at 0, 15, 30, 45 and 60 minutes after intraperitoneal inject in chow or HFD fed mice (n = 8). Data are shown as means ± s.e.m. **0.01 < P < 0.05, ***P < 0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1: The obese phenotype and fasting blood glucose of high-fat diet (HFD)-induced mice.(a) Food intake. The average grams food intake in WT and Gpr97−/− mice each month. (n = 8) (b) Body weight. The growth of body weight in WT and Gpr97−/− mice by chow or HFD feeding. (n = 6–8) (c) Intraperitoneal glucose tolerance test (ipGTT). The levels of blood glucose were detected at 0, 15, 30, 45 and 60 minutes after intraperitoneal inject in chow or HFD fed mice (n = 8). Data are shown as means ± s.e.m. **0.01 < P < 0.05, ***P < 0.01.
Mentions: The mice were fed with 60% calories in fat for 16 weeks to induce the metabolic syndrome. Metabolic phenotype, including food intake, body weight and glucose tolerance, was examined in mice. The quantity of food intake and body weight was recorded once a month. According to the collected data, there was no obvious difference in food intake between WT and Gpr97−/− HFD-fed mice (Fig. 1a). Although 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). Moreover, we used an intraperitoneal glucose tolerance test (ipGTT) to examine glucose tolerance in our mice model. The fasting blood glucose of HFD mice was much higher than that of the chow-fed mice from 15 min (P < 0.01), but there was no change after loss of Gpr97 in HFD mice compared with WT HFD mice (Fig. 1c). These data indicate that Gpr97 deficiency does not influence the body weight or glucose tolerance of HFD 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