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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

Microphotographs of the hepatic sections of control mice and Gpr97−/− mice.(a) The Oil-red staining of liver sections of WT and Gpr97−/− mice. (b) The PAS staining of liver sections of WT and Gpr97−/− mice. The lung sections were observed at 10× magnification under optical microscope.
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f4: Microphotographs of the hepatic sections of control mice and Gpr97−/− mice.(a) The Oil-red staining of liver sections of WT and Gpr97−/− mice. (b) The PAS staining of liver sections of WT and Gpr97−/− mice. The lung sections were observed at 10× magnification under optical microscope.

Mentions: The liver plays an important role in lipid metabolism, and hepatic steatosis was measured in an obese animal model8. HFD not only introduced obesity, but was also involved in glycometabolism and lipid metabolism in the liver. In our HFD mice, we used the Oil Red O stain to visualize hepatic neutral lipid accumulation in liver sections. The accumulation of lipid was severe in the livers of mice fed the HFD, but this accumulation was not significantly different between WT and Gpr97−/− HFD mice (Fig. 4a). Next, we measured the metabolism of carbohydrate in the liver by periodic acid-Schiff (PAS) staining, and found that there was more glycogen storage in the liver in HFD-fed mice. However, there was no difference between WT and Gpr97−/− mice (Fig. 4b). The loss of Gpr97, therefore, did not affect lipid or glycogen storage, or metabolic disorder, in the HFD-induced liver.


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)

Microphotographs of the hepatic sections of control mice and Gpr97−/− mice.(a) The Oil-red staining of liver sections of WT and Gpr97−/− mice. (b) The PAS staining of liver sections of WT and Gpr97−/− mice. The lung sections were observed at 10× magnification under optical microscope.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4: Microphotographs of the hepatic sections of control mice and Gpr97−/− mice.(a) The Oil-red staining of liver sections of WT and Gpr97−/− mice. (b) The PAS staining of liver sections of WT and Gpr97−/− mice. The lung sections were observed at 10× magnification under optical microscope.
Mentions: The liver plays an important role in lipid metabolism, and hepatic steatosis was measured in an obese animal model8. HFD not only introduced obesity, but was also involved in glycometabolism and lipid metabolism in the liver. In our HFD mice, we used the Oil Red O stain to visualize hepatic neutral lipid accumulation in liver sections. The accumulation of lipid was severe in the livers of mice fed the HFD, but this accumulation was not significantly different between WT and Gpr97−/− HFD mice (Fig. 4a). Next, we measured the metabolism of carbohydrate in the liver by periodic acid-Schiff (PAS) staining, and found that there was more glycogen storage in the liver in HFD-fed mice. However, there was no difference between WT and Gpr97−/− mice (Fig. 4b). The loss of Gpr97, therefore, did not affect lipid or glycogen storage, or metabolic disorder, in the HFD-induced liver.

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