Delayed Exercise Training Improves Obesity-Induced Chronic Kidney Disease by Activating AMPK Pathway in High-Fat Diet-Fed Mice.
Delayed Exercise Training Improves Obesity-Induced Chronic Kidney Disease by Activating AMPK Pathway in High-Fat Diet-Fed Mice.
复制标题
DOI：
10.3390/ijms22010350
复制
发表时间：
2020-12-31
影响因子：
5.6
通讯作者：
Declèves AE
中科院分区：
文献类型：
--
作者：
Juszczak F;Vlassembrouck M;Botton O;Zwakhals T;Decarnoncle M;Tassin A;Caron N;Declèves AE
运动训练现在被认为是一个有趣的治疗策略，在管理肥胖及其相关疾病。然而，仍然缺乏关于其对肥胖引起的慢性肾脏病（CKD）的影响的知识。在这里，我们研究了延迟的耐力运动训练（EET）协议的影响，以及在存在CKD的肥胖小鼠的潜在机制。喂食高脂饮食（HFD）或低脂饮食（LFD）12周的小鼠随后接受8周EET方案。在肥胖小鼠中延迟EET治疗可防止与卡路里摄入减少相关的体重增加。EET干预抵消了肥胖相关的疾病，包括葡萄糖耐量异常，胰岛素抵抗，血脂异常和肝脂肪变性。此外，我们的数据首次证明了EET对肥胖诱导的CKD的有益作用，如通过改善肥胖相关的肾小球病、肾小管间质纤维化、炎症和氧化应激所证明的。EET还防止近端小管中的肾脂质沉积。这些结果与肾组织中EET对AMPK通路的改善有关。AMPK介导的ACC和ULK-1的磷酸化特别增强，导致肥胖小鼠中EET的脂肪酸氧化增加和自噬改善。
Exercise training is now recognized as an interesting therapeutic strategy in managing obesity and its related disorders. However, there is still a lack of knowledge about its impact on obesity-induced chronic kidney disease (CKD). Here, we investigated the effects of a delayed protocol of endurance exercise training (EET) as well as the underlying mechanism in obese mice presenting CKD. Mice fed a high-fat diet (HFD) or a low-fat diet (LFD) for 12 weeks were subsequently submitted to an 8-weeks EET protocol. Delayed treatment with EET in obese mice prevented body weight gain associated with a reduced calorie intake. EET intervention counteracted obesity-related disorders including glucose intolerance, insulin resistance, dyslipidaemia and hepatic steatosis. Moreover, our data demonstrated for the first time the beneficial effects of EET on obesity-induced CKD as evidenced by an improvement of obesity-related glomerulopathy, tubulo-interstitial fibrosis, inflammation and oxidative stress. EET also prevented renal lipid depositions in the proximal tubule. These results were associated with an improvement of the AMPK pathway by EET in renal tissue. AMPK-mediated phosphorylation of ACC and ULK-1 were particularly enhanced leading to increased fatty acid oxidation and autophagy improvement with EET in obese mice.
登录
查看更多内容
影响因子：
4
作者：
de Carvalho, Francine Pereira;Moretto, Thais Ludmilla;Machado de Oliveira, Camila Aparecida
通讯作者：
Machado de Oliveira, Camila Aparecida
影响因子：
3.2
作者：
Farzanegi, Parvin;Dana, Amir;Azarbayjani, Mohammad Ali
通讯作者：
Azarbayjani, Mohammad Ali
影响因子：
5.7
作者：
Chun SK;Lee S;Yang MJ;Leeuwenburgh C;Kim JS
通讯作者：
Kim JS
影响因子：
4.5
作者：
Alex S;Boss A;Heerschap A;Kersten S
通讯作者：
Kersten S
影响因子：
15.9
作者：
Dugan, Laura L.;You, Young-Hyun;Sharma, Kumar
通讯作者：
Sharma, Kumar