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肌肉减少性肥胖、胰岛素抵抗及其对心血管和代谢后果的影响。

Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences.

机构信息

Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Korea University, Seoul 08308, Korea.

出版信息

Int J Mol Sci. 2020 Jan 13;21(2):494. doi: 10.3390/ijms21020494.

Abstract

The prevalence of sarcopenic obesity is increasing worldwide, particularly amongst aging populations. Insulin resistance is the core mechanism of sarcopenic obesity and is also associated with variable cardiometabolic diseases such as cardiovascular disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. Fat accumulation in muscle tissue promotes a proinflammatory cascade and oxidative stress, leading to mitochondrial dysfunction, impaired insulin signaling, and muscle atrophy. To compound the problem, decreased muscle mass aggravates insulin resistance. In addition, the crosstalk between myokines and adipokines leads to negative feedback, which in turn aggravates sarcopenic obesity and insulin resistance. In this review, we focus on the molecular mechanisms linking sarcopenic obesity and insulin resistance with various biological pathways. We also discuss the impact and mechanism of sarcopenic obesity and insulin resistance on cardiometabolic disease.

摘要

全世界范围内,肌少症性肥胖的患病率正在上升,尤其是在老龄化人群中。胰岛素抵抗是肌少症性肥胖的核心机制,也与各种心血管代谢疾病相关,如心血管疾病、2 型糖尿病和非酒精性脂肪性肝病。脂肪在肌肉组织中的堆积会促进促炎级联反应和氧化应激,导致线粒体功能障碍、胰岛素信号受损和肌肉萎缩。更糟糕的是,肌肉量减少会加重胰岛素抵抗。此外,肌肉因子和脂肪因子之间的相互作用会导致负反馈,从而进一步加重肌少症性肥胖和胰岛素抵抗。在这篇综述中,我们重点关注将肌少症性肥胖和胰岛素抵抗与各种生物途径联系起来的分子机制。我们还讨论了肌少症性肥胖和胰岛素抵抗对心血管代谢疾病的影响和机制。

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