Exercise retards ongoing adipose tissue fibrosis in diet-induced obese mice.
Exercise retards ongoing adipose tissue fibrosis in diet-induced obese mice.
复制标题
运动可以延缓饮食诱导的肥胖小鼠持续的脂肪组织纤维化。
DOI：
10.1530/ec-20-0643
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发表时间：
2021-03
影响因子：
2.9
通讯作者：
Yang W
中科院分区：
文献类型：
--
作者：
Li L;Wei Y;Fang C;Liu S;Zhou F;Zhao G;Li Y;Luo Y;Guo Z;Lin W;Yang W
运动已被推荐为改善肥胖患者葡萄糖代谢的重要策略。脂肪组织纤维化与炎症相关，并与肥胖中的葡萄糖代谢紊乱和胰岛素抵抗有关。然而，运动对脂肪组织纤维化进展的影响仍不清楚。本研究的目的是调查运动是否能延缓饮食诱导的肥胖小鼠脂肪组织纤维化的进展并改善葡萄糖稳态。为此，通过高脂饮食喂养 12 周诱导小鼠肥胖和脂肪组织纤维化，随后小鼠再接受 12 周的高脂饮食和运动干预。运动可以缓解高脂肪饮食引起的葡萄糖不耐受和胰岛素抵抗。持续的高脂肪饮食喂养加剧了胶原沉积，并进一步增加了脂肪组织中纤维化相关基因的表达。锻炼减弱或逆转了这些变化。此外，PPARγ 已被证明可以抑制脂肪组织纤维化，并且观察到运动后 PPARγ 会增加。而且，运动降低了脂肪纤维化中HIF-1α的表达，脂肪组织炎症受到抑制。总之，我们的数据表明，运动可以减弱甚至逆转脂肪组织纤维化的进展，为其对肥胖患者的葡萄糖代谢产生有益影响提供了一个合理的机制。
Exercise has been recommended as an important strategy to improve glucose metabolism in obesity. Adipose tissue fibrosis is associated with inflammation and is implicated in glucose metabolism disturbance and insulin resistance in obesity. However, the effect of exercise on the progression of adipose tissue fibrosis is still unknown. The aim of the present study was to investigate whether exercise retarded the progression of adipose tissue fibrosis and ameliorated glucose homeostasis in diet-induced obese mice. To do so, obesity and adipose tissue fibrosis in mice were induced by high-fat diet feeding for 12 weeks and the mice subsequently received high-fat diet and exercise intervention for another 12 weeks. Exercise alleviated high-fat diet-induced glucose intolerance and insulin resistance. Continued high-fat diet feeding exacerbated collagen deposition and further increased fibrosis-related gene expression in adipose tissue. Exercise attenuated or reversed these changes. Additionally, PPARγ, which has been shown to inhibit adipose tissue fibrosis, was observed to be increased following exercise. Moreover, exercise decreased the expression of HIF-1α in adipose fibrosis, and adipose tissue inflammation was inhibited. In conclusion, our data indicate that exercise attenuates and even reverses the progression of adipose tissue fibrosis, providing a plausible mechanism for its beneficial effects on glucose metabolism in obesity.