长期运动干预改善2型糖尿病肌萎缩的炎症机制研究进展

Research Progress of Inflammatory Mechanism of Long-term Exercise in Improvement of Muscle Atrophy in Patients with Type 2 Diabetes Mellitus

2型糖尿病肌萎缩会引起肌肉功能障碍,严重降低患者日常生活能力和生命质量。血清白细胞介素-6、C反应蛋白和肿瘤坏死因子-α等炎症介质的增加以及肌肉组织中核因子κB和信号转导及转录活化因子3等炎症通路的激活会引起肌细胞的减少或抑制肌细胞的分化,并参与2型糖尿病肌萎缩的发生发展。而长期运动可通过降低肌肉局部或全身炎症,提高骨骼肌质量,进而促进2型糖尿病肌萎缩的康复。但目前长期运动干预改善2型糖尿病肌萎缩的炎症机制仍不清楚。

Muscular atrophy in type 2 diabetes mellitus can cause muscle dysfunction,which will severely reduce the patient′s ability of daily living and quality of life.The elevated serum levels of inflammatory factors such as interleukin-6,C-reactive protein and tumor necrosis factor-α,as well as activation of inflammatory pathways like nuclear factorκB and signal transducer and activator of transcription 3 in muscle tissue,are involved in the occurrence and development of type 2 diabetic muscle atrophy by reducing muscle cell or inhibiting muscle cell differentiation.Long-term exercise can improve musculoskeletal muscle mass and promote the recovery of muscle atrophy in the patients with type 2 diabetes by reducing local muscle inflammation or systemic inflammation.However,the inflammatory mechanism of long-term exercise intervention to improve type 2 diabetic muscle atrophy is still unclear.