Department of Exercise Physiology, Beijing Sport University, Beijing, China; Department of Sports and Health Sciences, Nanjing Sport Institute, Nanjing, China.
Jiangsu Research Institute of Sports Science, Nanjing, China.
Life Sci. 2020 Feb 15;243:117246. doi: 10.1016/j.lfs.2019.117246. Epub 2020 Jan 2.
Obesity induce low-grade inflammation and elicit insulin resistance (IR), exercise training accompanied by a low-fat diet has been prescribed as part of the treatment for managing obesity and IR. The purpose of this study is to evaluate the effect of eccentric exercise accompanied by a low-fat diet on glycolipid metabolism, exercise capacity, and macrophage polarization in obesity-induced IR mice.
Mice were fed with 60% high fat diet (HFD) for 12 weeks and subsequently treated with eccentric exercise or/and dietary restriction for 8 weeks. Related biochemical index were examined both before and during intervention to evaluate the ability of glycolipid metabolism. Exercise capacity was measured to verify the results of biochemical index. At 12 weeks and 12 + 8 weeks, infiltration was observed by H&E staining in adipose tissue, and macrophage polarization was detected by Immunofluorescence staining and ELISA.
Eccentric exercise accompanied by a low-fat diet rescued obesity-induced IR and improved exercise capacity, which were associated with the inhibition of M1 macrophage polarization and the activation of M2 macrophage. These indicate that macrophage polarization provides the potential target of intervention for inflammation and IR in obesity.
肥胖会引起低度炎症，并导致胰岛素抵抗（IR），运动训练结合低脂饮食已被规定为肥胖和 IR 治疗的一部分。本研究的目的是评估伴随低脂饮食的离心运动对肥胖诱导的 IR 小鼠糖脂代谢、运动能力和巨噬细胞极化的影响。
将小鼠用 60%高脂肪饮食（HFD）喂养 12 周，然后用离心运动和/或饮食限制治疗 8 周。在干预前后检查相关生化指标，以评估糖脂代谢能力。测量运动能力以验证生化指标的结果。在 12 周和 12+8 周时，通过 H&E 染色观察脂肪组织的浸润，通过免疫荧光染色和 ELISA 检测巨噬细胞极化。
1）通过 12 周 HFD 喂养建立肥胖诱导的 IR 模型，伴随着运动能力受损和 M1 巨噬细胞增加，2）伴随低脂饮食的离心运动显著挽救肥胖诱导的 IR 并改善运动能力，3）伴随低脂饮食的离心运动显著抑制 M1 巨噬细胞极化并激活 M2 巨噬细胞。
伴随低脂饮食的离心运动挽救了肥胖诱导的 IR 并改善了运动能力，这与 M1 巨噬细胞极化的抑制和 M2 巨噬细胞的激活有关。这些表明巨噬细胞极化为肥胖相关炎症和 IR 提供了潜在的干预靶点。
