Limits...
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 major metabolites in serum in mice.(a) cholesterol, (b) glucose, (c) high-density lipoprotein (HDL), (d) low-density lipoprotein (LDL), (e) albumin, (f) carbamide, (g) creatinine, (h) triglyceride, (i) uric acid. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 0.01 < P < 0.05, ***P < 0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4835759&req=5

f2: Analysis of major metabolites in serum in mice.(a) cholesterol, (b) glucose, (c) high-density lipoprotein (HDL), (d) low-density lipoprotein (LDL), (e) albumin, (f) carbamide, (g) creatinine, (h) triglyceride, (i) uric acid. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 0.01 < P < 0.05, ***P < 0.01.

Mentions: To determine whether Gpr97 impacts on HFD-induced metabolic syndrome, the levels of some metabolites in serum were measured in mice. The levels of cholesterol, glucose, high-density cholesterol lipoprotein (HDL), and low-density cholesterol lipoprotein (LDL) in serum were increased in both HFD-fed WT and Gpr97−/− mice. However, there was no significant alteration of these serum parameters after Gpr97 deficiency in HFD-fed mice (Fig. 2a–d). The levels of albumin, carbamide, creatinine, triglyceride, and uric acid in serum were measured in mice. However, the HFD did not induce these indicators altering even in Gpr97−/− HFD mice (Fig. 2e–i). According to the metabolite analysis, Gpr97 is not involved in metabolic syndrome during HFD-induced obesity in 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 major metabolites in serum in mice.(a) cholesterol, (b) glucose, (c) high-density lipoprotein (HDL), (d) low-density lipoprotein (LDL), (e) albumin, (f) carbamide, (g) creatinine, (h) triglyceride, (i) uric acid. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 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

f2: Analysis of major metabolites in serum in mice.(a) cholesterol, (b) glucose, (c) high-density lipoprotein (HDL), (d) low-density lipoprotein (LDL), (e) albumin, (f) carbamide, (g) creatinine, (h) triglyceride, (i) uric acid. Data are shown as means ± s.e.m. (n = 8). *P < 0.05, ** 0.01 < P < 0.05, ***P < 0.01.
Mentions: To determine whether Gpr97 impacts on HFD-induced metabolic syndrome, the levels of some metabolites in serum were measured in mice. The levels of cholesterol, glucose, high-density cholesterol lipoprotein (HDL), and low-density cholesterol lipoprotein (LDL) in serum were increased in both HFD-fed WT and Gpr97−/− mice. However, there was no significant alteration of these serum parameters after Gpr97 deficiency in HFD-fed mice (Fig. 2a–d). The levels of albumin, carbamide, creatinine, triglyceride, and uric acid in serum were measured in mice. However, the HFD did not induce these indicators altering even in Gpr97−/− HFD mice (Fig. 2e–i). According to the metabolite analysis, Gpr97 is not involved in metabolic syndrome during HFD-induced obesity in 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