食品科学 ›› 2017, Vol. 38 ›› Issue (21): 279-286.doi: 10.7506/spkx1002-6630-201721044

• 专题论述 • 上一篇    下一篇

老年人肌少性肥胖的机制与运动营养调控研究进展

徐磊,李春艳,陈宁,范晶晶   

  1. (1.武汉体育学院研究生院,湖北?武汉 430079;2.武汉体育学院健康科学学院,天久运动营养食品研发中心,湖北?武汉 430079)
  • 出版日期:2017-11-15 发布日期:2017-11-01
  • 基金资助:
    国家自然科学基金面上项目(31571228);国家体育总局科教司科学研究项目(2014B093); 湖北省高等学校优秀中青年科技创新团队项目(T201624);湖北省体育教育与健康促进学科群项目

Exercise and Nutrition Interventions of Sarcopenic Obesity and Underlying Mechanisms

XU Lei,LI Chunyan,CHEN Ning,FAN Jingjing   

  1. (1. Graduate School, Wuhan Sports University, Wuhan 430079, China; 2. Tianjiu Research and Development Center for Exercise Nutrition and Foods, College of Health Science, Wuhan Sports University, Wuhan 430079, China)
  • Online:2017-11-15 Published:2017-11-01

摘要: 老年人肌少性肥胖(sarcopenic obesity,SO)是一种伴随着肥胖的骨骼肌质量和功能下降的老年性疾病,多发于老年人群而严重影响其生活质量。大量研究结果表明随着年龄的增长,即使体质量不变,老年人身体组成也会逐渐改变,肌肉质量功能下降,脂肪比例上升且主要堆积在肌肉组织、内脏器官,整体表现为肌肉脂肪量上升、炎症因子增多、生长激素水平下降、营养摄入不足、活动量降低、神经元功能下降以及胰岛素抵抗等,这些现象都与SO相关。从分子水平阐述其相关机制,研究者发现骨骼肌蛋白质合成与降解、骨骼肌糖脂代谢以及相关细胞因子均参与SO代谢通路的调控。运动干预、热量限制及蛋白质、VD、β-羟基-β-甲基丁酸盐、肌酸和乳清蛋白的摄入均可在一定程度上起到防治SO的效果。由于国内外对于SO的判断标准、发病机制以及防治手段仍不统一,给SO研究带来了较大难度。本文对国内外最新研究报道进行整理总结,从SO的定义、引起因素、涉及的细胞信号调控通路以及防治策略(运动或营养食品干预)等方面进行了综述,为SO治疗提供新思路。

关键词: 肌少性肥胖, 病理机制, 信号调控通路, 防治策略

Abstract: Sarcopenic obesity (SO) is a progressive disease characterized by obesity accompanied by declining skeletal muscle mass and/or strength in aging populations, which seriously affects the quality of life of patients. A large number of studies have shown that the body composition of the elderly could gradually change with age, even if the body weight remains at the same level, skeletal muscle mass and functions could decrease and fat deposition could increase mainly in muscle tissues and visceral organs, leading to increased accumulation of intramuscular fat, accelerated secretion of inflammatory phenomena, reduced level of growth hormones, deficient intake of nutrients, increased daily physical inactivity, degenerated neuronal function, and improved insulin resistance, which are highly associated with sarcopenic obesity. Based on the molecular underlying molecular mechanisms, protein synthesis and degradation, glucose and lipid metabolism and related cytokines in skeletal muscle are involved in the regulation of skeletal muscle metabolism during sarcopenic obesity. Exercise intervention, calorie restriction, and consumption of proteins, vitamin D, β-hydroxy-β-methyl-butyrate (HMB), creatine and whey protein can play an important role in the prevention and treatment of sarcopenic obesity. Although the number of population with sarcopenic obesity increases, the pathogenesis of sarcopenic obesity is inconsistently understood and inconsistent evaluation criteria and prevention and treatment strategies for this disease are used by researchers, causing great difficulties in studying sarcopenic obesity. In this article, we summarize and discuss the literature to date regarding the definition, pathogenesis and related signal pathways of sarcopenic obesity, as well as the corresponding prevention and treatment strategies (exercise or nutrition interventions), which will provide a novel insight into the prevention and treatment of sarcopenic obesity.

Key words: sarcopenic obesity, pathogenesis, signal pathway, prevention and treatment strategies

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