Department of Nutritional Sciences, Auburn University, Auburn, AL, 36849, USA.
Department of Anatomy Physiology and Pharmacology, Auburn University, Auburn, AL, 36849, USA.
Curr Nutr Rep. 2024 Sep;13(3):500-515. doi: 10.1007/s13668-024-00555-7. Epub 2024 Jul 8.
The global obesity epidemic has become a major public health concern, necessitating comprehensive research into its adverse effects on various tissues within the human body. Among these tissues, skeletal muscle has gained attention due to its susceptibility to obesity-related alterations. Mitochondria are primary source of energy production in the skeletal muscle. Healthy skeletal muscle maintains constant mitochondrial content through continuous cycle of synthesis and degradation. However, obesity has been shown to disrupt this intricate balance. This review summarizes recent findings on the impact of obesity on skeletal muscle mitochondria structure and function. In addition, we summarize the molecular mechanism of mitochondrial quality control systems and how obesity impacts these systems. RECENT FINDINGS: Recent findings show various interventions aimed at mitigating mitochondrial dysfunction in obese model, encompassing strategies including caloric restriction and various dietary compounds. Obesity has deleterious effect on skeletal muscle mitochondria by disrupting mitochondrial biogenesis and dynamics. Caloric restriction, omega-3 fatty acids, resveratrol, and other dietary compounds enhance mitochondrial function and present promising therapeutic opportunities.
全球肥胖症流行已成为主要公共卫生关注点,需要全面研究其对人体各种组织的不良影响。在这些组织中,骨骼肌因易受肥胖相关改变的影响而受到关注。线粒体是骨骼肌能量产生的主要来源。健康的骨骼肌通过不断的合成和降解循环来维持恒定的线粒体含量。然而,肥胖已被证明会破坏这种复杂的平衡。本综述总结了肥胖对骨骼肌线粒体结构和功能的影响的最新发现。此外,我们总结了线粒体质量控制系统的分子机制以及肥胖如何影响这些系统。最新发现:最近的研究结果表明,各种旨在减轻肥胖模型中线粒体功能障碍的干预措施,包括热量限制和各种饮食化合物。肥胖通过破坏线粒体生物发生和动力学对骨骼肌线粒体产生有害影响。热量限制、ω-3 脂肪酸、白藜芦醇和其他饮食化合物可增强线粒体功能,提供有前景的治疗机会。