She Ying, Ma Yun, Zou Pei, Peng Yang, An Yong, Chen Hang, Luo Peng, Wei Shaofeng
The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Provincial Engineering Research Center of Ecological Food Innovation, Collaborative Innovation Center for Prevention and Control of Endemic and Ethnic Regional Diseases Co-Constructed by the Province and Ministry, School of Public Health, Guizhou Medical University, Guiyang 561113, China.
State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang 550025, China.
Life (Basel). 2024 Jun 21;14(7):784. doi: 10.3390/life14070784.
Type 2 diabetes mellitus (T2DM) is a burgeoning public health challenge worldwide. Individuals with T2DM are at increased risk for skeletal muscle atrophy, a serious complication that significantly compromises quality of life and for which effective prevention measures are currently inadequate. Emerging evidence indicates that systemic and local inflammation stemming from the compromised intestinal barrier is one of the crucial mechanisms contributing to skeletal muscle atrophy in T2DM patients. Notably, natural plant polysaccharides were found to be capable of enhancing intestinal barrier function and mitigating secondary inflammation in some diseases. Herein, we hypothesized that polysaccharide (GFP), one of the major plant polysaccharides, could prevent skeletal muscle atrophy in T2DM via regulating intestinal barrier function and inhibiting systemic and local inflammation. Using a well-established T2DM rat model, we demonstrated that GFP was able to not only prevent hyperglycemia and insulin resistance but also repair intestinal mucosal barrier damage and subsequent inflammation, thereby alleviating the skeletal muscle atrophy in the T2DM rat model. Additionally, the binding free energy analysis and molecular docking of monosaccharides constituting GFP were further expanded for related targets to uncover more potential mechanisms. These results provide a novel preventative and therapeutic strategy for T2DM patients.
2型糖尿病（T2DM）是全球范围内日益严峻的公共卫生挑战。T2DM患者骨骼肌萎缩风险增加，这是一种严重并发症，显著影响生活质量，而目前有效的预防措施并不充足。新出现的证据表明，肠道屏障受损引发的全身和局部炎症是导致T2DM患者骨骼肌萎缩的关键机制之一。值得注意的是，人们发现天然植物多糖能够增强肠道屏障功能并减轻某些疾病中的继发性炎症。在此，我们假设主要植物多糖之一的多糖（GFP）可通过调节肠道屏障功能并抑制全身和局部炎症来预防T2DM中的骨骼肌萎缩。使用成熟的T2DM大鼠模型，我们证明GFP不仅能够预防高血糖和胰岛素抵抗，还能修复肠道黏膜屏障损伤及随后的炎症，从而减轻T2DM大鼠模型中的骨骼肌萎缩。此外，对构成GFP的单糖进行结合自由能分析和分子对接，进一步拓展至相关靶点，以揭示更多潜在机制。这些结果为T2DM患者提供了一种新的预防和治疗策略。
