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The innate immune system is associated with the development of local inflammation. Neutrophils play an essential role in the development of the adipose tissue ( AT) inflammation associated with obesity by producing elastase, which can promote the activation and infiltration of macrophages. Exercise training attenuates AT inflammation via suppression of macrophage infiltration. However, the mechanisms driving this phenomenon remains to be elucidated. Here, we evaluated the effects of exercise training on the infiltration of neutrophils and elastase expression in an obese mouse model. Four-week-old male C57 BL/6J mice were randomly assigned to one of three groups that either received a normal diet ( ND) plus sedentary activity ( n = 15), a high-fat diet ( HFD) plus sedentary activity ( n = 15), or a HFD plus exercise training ( n = 15). Mice were fed the ND or HFD from the age of 4 weeks until 20 weeks. Mice in the exercise group ran on a treadmill for 60 min/day, 5 days/week over the same experimental period. Mice fed with the HFD had increased content of macrophages in the AT and increased inflammatory cytokine mRNA levels, which were reduced by exercise training. Similarly, AT from the HFD sedentary mice contained more neutrophils than AT from the ND mice, and the amount of neutrophils in this tissue in HFD-fed mice was lowered by exercise training. The mRNA levels of neutrophil elastase in AT were lower in the HFD exercise-trained mice than those in the HFD sedentary mice. These results suggest that exercise training plays a critical role in reducing macrophage infiltration and AT inflammation by regulating the infiltration of neutrophils. [ABSTRACT FROM AUTHOR]

Although nonalcoholic steatohepatitis (NASH) is an important component of the metabolic syndrome, scavenger receptor CD36 also modulates NASH development. This study aimed to clarify whether exercise training suppresses CD36 expression in a mouse model of NASH. Male C57BL/6 mice were divided into four groups: normal diet (ND) sedentary, ND exercise, high‐fat diet and high‐fructose water (HFF) sedentary, and HFF exercise groups. The exercise groups were trained on a motorized treadmill at running speeds of 15–20 m/min for 60 min/day, 5 times/week for 16 weeks. CD36 cell surface expression of hepatic resident macrophages, peroxisome proliferator‐activated receptor (PPAR)‐γ protein, and mRNA levels in the liver were increased in HFF sedentary mice but were attenuated in HFF exercise mice. Hepatic resident macrophages were significantly lower in HFF exercise mice than in HFF sedentary mice. Our findings indicated that exercise training reduced macrophage quantity in the liver, and downregulated CD36 and PPAR‐γ expression in liver and macrophages. Exercise training attenuated cell surface expression of CD36 in hepatic resident macrophages in the NASH model mice. Exercise training‐induced reduction in CD36 expression might be regulated by the down‐regulation of PPAR‐gamma. [ABSTRACT FROM AUTHOR]

Highlights: [•] We examined the effects of exercise on adipose tissue fibrosis improvement in obese mice. [•] Collagen deposition in adipose tissue was suppressed by exercise training. [•] Exercise training induced reduction of macrophage infiltration in the adipose tissue. [•] Exercise plays a role in attenuating tissue fibrosis via reduction of macrophage. [ABSTRACT FROM AUTHOR]