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通过力量训练和耐力训练改善肥胖相关的骨骼肌胰岛素抵抗。

Improvement of obesity-linked skeletal muscle insulin resistance by strength and endurance training.

作者信息

Di Meo Sergio, Iossa Susanna, Venditti Paola

机构信息

Dipartimento di BiologiaUniversità di Napoli 'Federico II', Napoli, Italy

Dipartimento di BiologiaUniversità di Napoli 'Federico II', Napoli, Italy.

出版信息

J Endocrinol. 2017 Sep;234(3):R159-R181. doi: 10.1530/JOE-17-0186.

DOI:10.1530/JOE-17-0186
PMID:28778962
Abstract

Obesity-linked insulin resistance is mainly due to fatty acid overload in non-adipose tissues, particularly skeletal muscle and liver, where it results in high production of reactive oxygen species and mitochondrial dysfunction. Accumulating evidence indicates that resistance and endurance training alone and in combination can counteract the harmful effects of obesity increasing insulin sensitivity, thus preventing diabetes. This review focuses the mechanisms underlying the exercise role in opposing skeletal muscle insulin resistance-linked metabolic dysfunction. It is apparent that exercise acts through two mechanisms: (1) it stimulates glucose transport by activating an insulin-independent pathway and (2) it protects against mitochondrial dysfunction-induced insulin resistance by increasing muscle antioxidant defenses and mitochondrial biogenesis. However, antioxidant supplementation combined with endurance training increases glucose transport in insulin-resistant skeletal muscle in an additive fashion only when antioxidants that are able to increase the expression of antioxidant enzymes and/or the activity of components of the insulin signaling pathway are used.

摘要

与肥胖相关的胰岛素抵抗主要是由于非脂肪组织(特别是骨骼肌和肝脏)中的脂肪酸过载,这会导致活性氧的大量产生和线粒体功能障碍。越来越多的证据表明,单独或联合进行抗阻训练和耐力训练可以抵消肥胖的有害影响,提高胰岛素敏感性,从而预防糖尿病。本综述聚焦于运动在对抗骨骼肌胰岛素抵抗相关代谢功能障碍中作用的潜在机制。显然,运动通过两种机制发挥作用:(1)通过激活一条不依赖胰岛素的途径来刺激葡萄糖转运;(2)通过增强肌肉抗氧化防御和线粒体生物合成来抵御线粒体功能障碍诱导的胰岛素抵抗。然而,只有当使用能够增加抗氧化酶表达和/或胰岛素信号通路成分活性的抗氧化剂时,抗氧化剂补充与耐力训练联合使用才能以相加的方式增加胰岛素抵抗骨骼肌中的葡萄糖转运。

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