Tammineni Eshwar R, Manno Carlo, Oza Goldie, Figueroa Lourdes
Department of Physiology and Biophysics, Rush University, Chicago, USA.
Department of Physiology and Biophysics, Rush University, Chicago, USA.
Mol Cell Endocrinol. 2025 Apr 1;599:112466. doi: 10.1016/j.mce.2025.112466. Epub 2025 Jan 21.
The incidence and prevalence of muscular disorders and of type 2 diabetes (T2D) is increasing and both represent highly significant healthcare problems, both economically and compromising quality of life. Interestingly, skeletal muscle dysfunction and T2D share some commonalities including dysregulated glucose homeostasis, increased oxidative stress, dyslipidemia, and cytokine alterations. Several lines of evidence have hinted to a relationship between skeletal muscle dysfunction and T2D. For instance, T2D affects skeletal muscle morphology, functionality, and overall health through altered protein metabolism, impaired mitochondrial function, and ultimately cell viability. Conversely, humans suffering from myopathies and their experimental models demonstrated increased incidence of T2D through altered muscle glucose disposal function due to abnormal calcium homeostasis, compromised mitochondrial function, dyslipidemia, increased inflammatory cytokines and fiber size alterations and disproportions. Lifestyle modifications are essential for improving and maintaining mobility and metabolic health in individuals suffering from myopathies along with T2D. In this review, we updated current literature evidence on clinical incidence of T2D in inflammatory, mitochondrial, metabolic myopathies, and muscular dystrophies and further discussed the molecular basis of these skeletal muscle disorders leading to T2D.
肌肉疾病和2型糖尿病(T2D)的发病率和患病率都在上升,这两者在经济方面以及对生活质量的影响上都代表着极为重大的医疗保健问题。有趣的是,骨骼肌功能障碍和T2D存在一些共同之处,包括葡萄糖稳态失调、氧化应激增加、血脂异常和细胞因子改变。几条证据线索都暗示了骨骼肌功能障碍与T2D之间的关系。例如,T2D通过改变蛋白质代谢、损害线粒体功能并最终影响细胞活力,从而影响骨骼肌形态、功能和整体健康。相反,患有肌病的人和他们的实验模型表明,由于钙稳态异常、线粒体功能受损、血脂异常、炎性细胞因子增加以及纤维大小改变和比例失调,导致肌肉葡萄糖处理功能改变,T2D的发病率增加。生活方式的改变对于改善和维持患有肌病以及T2D的个体的活动能力和代谢健康至关重要。在这篇综述中,我们更新了关于炎症性、线粒体性、代谢性肌病和肌肉营养不良中T2D临床发病率的现有文献证据,并进一步讨论了这些导致T2D的骨骼肌疾病的分子基础。