고지방식이로 유도된 비만 마우스의 지방조직에서 일회성 운동이대식세포 표현형 비율 변화에 미치는 영향

PURPOSE: Exercise in known to inhibit M1 macrophage (M1ф) differentiation, and increase in M2 macrophage (M2ф) and inhibition of M1ф in adipose tissue are known to reduce obesity. However, studies on the effects of exercise are very limited and it has not yet confirmed whether the polarization of M1...

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Veröffentlicht in:Exercise science (Seoul, Korea) 2018, 27(3), , pp.232-243
1. Verfasser: 백경완
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Sprache:kor
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Zusammenfassung:PURPOSE: Exercise in known to inhibit M1 macrophage (M1ф) differentiation, and increase in M2 macrophage (M2ф) and inhibition of M1ф in adipose tissue are known to reduce obesity. However, studies on the effects of exercise are very limited and it has not yet confirmed whether the polarization of M1ф/M2ф actually changes. Therefore, I tried to confirm the M1ф/M2ф polarization in the real change in single bout of exercise. METHODS: Male C57BL/6 mice were divided into four groups; normal diet (ND) control (n=7), ND exercise (n=7), high-fat diet (HFD) control (n=7), and HFD exercise (n=7) groups. All exercise mice ran on a treadmill at 15 m/min for 60 min for single bout. All animals were sacrificed two hours after single-bout of exercise and adipose tissue was isolated. Adipocytes were extracted from isolated adipose tissue and FACS was performed. RESULTS: Single bout of exercise in high-fat diet induced obese mice did not actually increase M2ф polarization in adipose tissue. Rather, the expression of M1ф was significantly higher than that of the other groups. However, expression of M2ф-related genes (Arg1) was highest in HFD-EX compared to ND control and HFD control. CONCLUSIONS: Despite the increase of M1ф due to obesity, the expression of M2ф-related gene Arg1 was found to be increased by exercise regardless of the high-fat diet. These results suggest for the first time that a single bout of exercise can independently affect the change in M1ф/M2ф phenotypic ratio regardless of obesity or high-fat diet. KCI Citation Count: 2
ISSN:1226-1726
2384-0544
DOI:10.15857/ksep.2018.27.3.232