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抗阻运动训练可改善高脂肪饮食喂养小鼠脂肪和肌肉组织的代谢和炎症控制。

Resistance Exercise Training Improves Metabolic and Inflammatory Control in Adipose and Muscle Tissues in Mice Fed a High-Fat Diet.

机构信息

Faculty of Sports Science, Ningbo University, Ningbo 315211, China.

Graduate Program in Health Science, Medical School, Universidade do Extremo Sul Catarinense, Criciúma 88806-000, SC, Brazil.

出版信息

Nutrients. 2022 May 24;14(11):2179. doi: 10.3390/nu14112179.

DOI:10.3390/nu14112179
PMID:35683979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9182921/
Abstract

This study investigates whether ladder climbing (LC), as a model of resistance exercise, can reverse whole-body and skeletal muscle deleterious metabolic and inflammatory effects of high-fat (HF) diet-induced obesity in mice. To accomplish this, Swiss mice were fed for 17 weeks either standard chow (SC) or an HF diet and then randomly assigned to remain sedentary or to undergo 8 weeks of LC training with progressive increases in resistance weight. Prior to beginning the exercise intervention, HF-fed animals displayed a 47% increase in body weight (BW) and impaired ability to clear blood glucose during an insulin tolerance test (ITT) when compared to SC animals. However, 8 weeks of LC significantly reduced BW, adipocyte size, as well as glycemia under fasting and during the ITT in HF-fed rats. LC also increased the phosphorylation of Akt and AMPK and reduced tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL1-β) contents in the quadriceps muscles of HF-fed mice. Additionally, LC reduced the gene expression of inflammatory markers and attenuated HF-diet-induced NADPH oxidase subunit gp91phox in skeletal muscles. LC training was effective in reducing adiposity and the content of inflammatory mediators in skeletal muscle and improved whole-body glycemic control in mice fed an HF diet.

摘要

本研究旨在探讨爬梯(LC)作为一种抗阻运动模型,是否能逆转高脂肪(HF)饮食诱导肥胖小鼠全身和骨骼肌的有害代谢和炎症效应。为此,将瑞士小鼠分别用标准饲料(SC)或 HF 饲料喂养 17 周,然后随机分为保持安静或进行 8 周的 LC 训练,阻力重量逐渐增加。在开始运动干预之前,与 SC 动物相比,HF 喂养的动物体重增加了 47%,并且在胰岛素耐量试验(ITT)期间清除血糖的能力受损。然而,8 周的 LC 显著降低了 HF 喂养大鼠的 BW、脂肪细胞大小以及空腹和 ITT 期间的血糖。LC 还增加了 HF 喂养小鼠股四头肌中 Akt 和 AMPK 的磷酸化,并降低了肿瘤坏死因子-α(TNF-α)和白细胞介素 1β(IL1-β)的含量。此外,LC 降低了炎症标志物的基因表达,并减弱了 HF 饮食诱导的骨骼肌中 NADPH 氧化酶亚基 gp91phox。LC 训练有效降低了肥胖小鼠的脂肪含量和骨骼肌中炎症介质的含量,并改善了 HF 饮食喂养小鼠的全身血糖控制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29c8/9182921/2f50de5ba66f/nutrients-14-02179-g007.jpg
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