生物技术进展 ›› 2022, Vol. 12 ›› Issue (6): 861-868.DOI: 10.19586/j.2095-2341.2022.0081

• 进展评述 • 上一篇    下一篇

肥胖诱导的骨骼肌萎缩机制研究进展

郭婧雅1(), 张萍1, 赵雨菡1, 李梦杰1, 黄昆仑1,2,3(), 仝涛1,2,3()   

  1. 1.中国农业大学食品科学与营养工程学院,精准营养与食品质量重点实验室,教育部功能乳品重点实验室,北京 100083
    2.农业农村部转基因生物安全评价重点实验室(食品安全),北京 100083
    3.食品质量与安全北京实验室,北京 100083
  • 收稿日期:2022-05-19 接受日期:2022-07-08 出版日期:2022-11-25 发布日期:2022-11-30
  • 通讯作者: 黄昆仑,仝涛
  • 作者简介:郭婧雅 E-mail: guojy2017@126.com
  • 基金资助:
    北京市自然科学基金项目(7222249);山东省自然科学基金青年基金项目(ZR2021QC118);中国农业大学2115人才工程资助项目

Advances on the Mechanism of Obesity-induced Skeletal Muscle Atrophy

Jingya GUO1(), Ping ZHANG1, Yuhan ZHAO1, Mengjie LI1, Kunlun HUANG1,2,3(), Tao TONG1,2,3()   

  1. 1.Key Laboratory of Precision Nutrition and Food Quality,Key Laboratory of Functional Dairy Products,Ministry of Education,School of Food Science and Nutrition Engineering,China Agricultural University,Beijing 100083,China
    2.Key Laboratory of Safety Evaluation of Genetically Modified Organisms (Food Safety),Ministry of Agriculture and Rural Affairs,Beijing 100083,China
    3.Beijing Laboratory of Food Quality and Safety,Beijing 100083,China
  • Received:2022-05-19 Accepted:2022-07-08 Online:2022-11-25 Published:2022-11-30
  • Contact: Kunlun HUANG,Tao TONG

摘要:

骨骼肌是人体氨基酸和蛋白质的主要贮存、代谢库,其正常功能和代谢过程受到多种病理因素的影响。骨骼肌萎缩发生于骨骼肌稳态严重失衡状态下,对患者生活和社会医疗造成了沉重负担。近年来,由于世界肥胖人群数量激增,肥胖诱导的骨骼肌萎缩正日益成为公共卫生的严峻挑战之一。肥胖诱导的骨骼肌萎缩过程涉及多种信号分子或通路的改变,如泛素蛋白酶系统、自噬溶酶体系统、胰岛素/IGF1-PI3K-Akt、肌肉生长抑制素、白细胞介素-6、肿瘤坏死因子等;这些信号分子或通路在肥胖状态下被激活或抑制后,可共同影响蛋白质合成/分解平衡进而造成骨骼肌萎缩。基于上述信号分子或通路,系统总结并讨论了肥胖诱导的骨骼肌萎缩机制,以期为寻找缓解/治疗肥胖诱导的肌萎缩靶点和进一步开发利用天然植物化学物提供理论依据。

关键词: 肥胖, 肌萎缩, 骨骼肌, 蛋白质合成/分解

Abstract:

Skeletal muscle is the main storage and metabolic reservoir of amino acids and proteins in the body, and its normal function and metabolic processes are affected by a variety of pathological factors. Skeletal muscle atrophy occurs in a state of severe imbalance in skeletal muscle homeostasis, which imposes a heavy burden on patients' lives and social and medical care. In recent years, obesity-induced skeletal muscle atrophy is increasingly becoming a serious public health challenge due to the proliferation of obesity in the world. Obesity-induced skeletal muscle atrophy involves changes in various signaling molecules or pathways, such as ubiquitin protease system, autophagy-lysosomal system, insulin/IGF1-PI3K-Akt, myostatin, interleukin-6, tumor necrosis factor, etc. After these signal molecules or pathways are activated or inhibited in the state of obesity, they can jointly affect the balance of protein synthesis/catabolism and further cause skeletal muscle atrophy. Based on the above-mentioned signaling molecules or pathways, this study systematically summarized and discussed the mechanism underlying obesity-induced skeletal muscle atrophy, hoping to provide theoretical references for exploring preventive or therapeutic targets of obesity-induced muscle atrophy, and to extend the development and utilization of natural phytochemicals.

Key words: obesity, muscle atrophy, skeletal muscle, protein synthesis/catabolism

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