Interleukin-6 mediated exercise-induced alleviation of adiposity and hepatic steatosis in mice.
Interleukin-6 mediated exercise-induced alleviation of adiposity and hepatic steatosis in mice.
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白介素 6 介导运动引起的小鼠肥胖和肝脂肪变性的缓解
DOI：
10.1136/bmjdrc-2020-001431
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发表时间：
2021-04
影响因子：
4.1
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Li L;Huang C;Yin H;Zhang X;Wang D;Ma C;Li J;Zhao Y;Li X
简介 运动训练已被证明是对抗肥胖和非酒精性脂肪肝的最有效策略。然而，运动会促进脂肪组织量的减少，并通过仍不清楚的机制改善与肥胖相关的肝脏脂肪变性。研究设计和方法为了研究白细胞介素6（IL-6）在跑步机跑步期间高脂饮食（HFD）引起的肥胖和肝脂肪变性中的作用，将IL-6敲除（IL-6 KO）小鼠和野生型（WT）小鼠随机分为瘦型组、肥胖组（喂食HFD）和训练肥胖组（喂食HFD并进行运动训练）。结果经过20周的HFD喂养和8周的跑步机跑步后，我们发现运动明显减少了HFD引起的体重增加，抑制了WT小鼠内脏脂肪组织（VAT）和皮下脂肪组织（SAT）的扩张，并且几乎完全逆转了肥胖相关的肝内脂肪堆积。然而，IL-6 敲除 (IL-6 KO) 小鼠难以接受跑步机训练对体重、VAT 和 SAT 质量升高以及肝脂肪变性的益处。此外，与未训练的小鼠相比，接受运动训练的 WT 小鼠的 VAT 和 SAT 中一组脂肪分解相关和生热相关基因（包括 ATGL、HSL 和 PGC-1α）上调，而在 IL-6 KO 小鼠中未观察到这种情况。此外，运动训练导致WT小鼠肝脏过氧化物酶体增殖物激活受体γ（PPAR-γ）表达显着抑制，而在IL-6 KO小鼠中没有注意到这些影响。结论这些结果表明IL-6参与预防运动训练期间的肥胖和肝脏脂肪堆积。这些抗肥胖作用的机制可能与白色脂肪组织中脂肪分解和生热作用的增强有关。运动训练对肝脏脂肪变性的改善可能受益于IL-6对PPAR-γ表达的显着抑制。
Introduction Exercise training has been shown to be the most effective strategy to combat obesity and non-alcoholic fatty liver disease. However, exercise promotes loss of adipose tissue mass and improves obesity-related hepatic steatosis through mechanisms that remain obscure. Research design and methods To study the role of interleukin-6 (IL-6) in high-fat diet (HFD)-induced adiposity and hepatic steatosis during treadmill running, IL-6 knockout (IL-6 KO) mice and wild-type (WT) mice were randomly divided into lean, obese (fed a HFD) and trained obese groups (fed a HFD and exercise trained). Results After 20 weeks of HFD feeding and 8 weeks of treadmill running, we found that exercise obviously reduced HFD-induced body weight gain, inhibited visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) expansion and almost completely reversed obesity-related intrahepatic fat accumulation in WT mice. However, IL-6 knockout (IL-6 KO) mice are refractory to the benefits of treadmill training on body weight, VAT and SAT mass elevation, and hepatic steatosis. Moreover, a panel of lipolytic-related and thermogenic-related genes, including ATGL, HSL and PGC-1α, was upregulated in the VAT and SAT of WT mice that received exercise training compared with untrained mice, which was not observed in IL-6 KO mice. In addition, exercise training resulted in a significant inhibition of hepatic peroxisome proliferator-activated receptor gamma (PPAR-γ) expression in WT mice, and these effects were not noted in IL-6 KO mice. Conclusion These results revealed that IL-6 is involved in the prevention of obesity and hepatic fat accumulation during exercise training. The mechanisms underlying these antiobesity effects may be associated with enhanced lipolysis and thermogenesis in white adipose tissue. The improvement in hepatic steatosis by exercise training may benefit from the marked inhibition of PPAR-γ expression by IL-6.
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DOI：
10.1002/oby.20671
发表时间：
2014-04
期刊：
Obesity (Silver Spring, Md.)
影响因子：
--
作者：
Gawronska-Kozak B;Staszkiewicz J;Gimble JM;Kirk-Ballard H
通讯作者：
Kirk-Ballard H
影响因子：
15.9
作者：
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Gonzalez, FJ
影响因子：
3.7
作者：
Knudsen, Jenny Dahl;Andersen, Stig Ejdrup
通讯作者：
Andersen, Stig Ejdrup
影响因子：
5.5
作者：
McKie, Greg L.;Medak, Kyle D.;Wright, David C.
通讯作者：
Wright, David C.
DOI：
10.1016/j.metabol.2017.11.009
发表时间：
2018-04
期刊：
Metabolism: clinical and experimental
影响因子：
--
作者：
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通讯作者：
Symonds ME