Losasso Marina Ribas, Parussolo Maria Luiza Cesto, Oliveira Silva Antony, Direito Rosa, Quesada Karina, Penteado Detregiachi Claudia Rucco, Bechara Marcelo Dib, Méndez-Sánchez Nahum, Abenavoli Ludovico, Araújo Adriano Cressoni, de Alvares Goulart Ricardo, Guiger Elen Landgraf, Fornari Laurindo Lucas, Maria Barbalho Sandra
Department of Biochemistry and Pharmacology, School of Medicine, Universidade de Marília (UNIMAR), Marília 17525-902, SP, Brazil.
Laboratory of Systems Integration Pharmacology, Clinical and Regulatory Science, Research Institute for Medicines, Universidade de Lisboa (iMed.ULisboa), Av. Prof. Gama Pinto, 1649-003 Lisbon, Portugal.
Int J Mol Sci. 2025 May 14;26(10):4673. doi: 10.3390/ijms26104673.
Metabolic-Associated Fatty Liver Disease (MAFLD) is a public health concern that is constantly expanding, with a fast-growing prevalence, and it affects about a quarter of the world's population. This condition is a significant risk factor for cardiovascular, hepatic, and oncologic diseases, such as hypertension, hepatoma, and atherosclerosis. Sarcopenia was long considered to be an aging-related syndrome, but today, it is acknowledged to be secondarily related to chronic diseases such as metabolic syndrome, cardiovascular conditions, and liver diseases, among other comorbidities associated with insulin resistance and chronic inflammation, besides inactivity and poor nutrition. The physiopathology involving MAFLD and sarcopenia has still not been solved. Inflammation, oxidative stress, mitochondrial dysfunction, and insulin resistance seem to be some of the keys to this relationship since this hormone target is mainly the skeletal muscle. This review aimed to comprehensively discuss the main metabolic and physiological pathways involved in these conditions. MAFLD and sarcopenia are interconnected by a complex network of pathophysiological mechanisms, such as insulin resistance, skeletal muscle tissue production capacity, chronic inflammatory state, oxidative stress, and mitochondrial dysfunction, which are the main contributors to this relationship. In addition, in a clinical analysis, patients with sarcopenia and MAFLD manifest more severe hepatitis fibrosis when compared to patients with only MAFLD. These patients, with both disorders, also present clinical improvement in their MAFLD when treated for sarcopenia, reinforcing the association between them. Lifestyle changes accompanied by non-pharmacological interventions, such as dietary therapy and increased physical activity, undoubtedly improve this scenario.
代谢相关脂肪性肝病(MAFLD)是一个日益受到关注的公共卫生问题,其患病率迅速上升,影响着全球约四分之一的人口。这种疾病是心血管、肝脏和肿瘤疾病的重要危险因素,如高血压、肝癌和动脉粥样硬化。肌肉减少症长期以来被认为是一种与衰老相关的综合征,但如今人们认识到它与慢性疾病如代谢综合征、心血管疾病和肝脏疾病等继发性相关,这些疾病还伴有胰岛素抵抗和慢性炎症等其他合并症,此外还与缺乏运动和营养不良有关。MAFLD和肌肉减少症的生理病理学仍未得到解决。炎症、氧化应激、线粒体功能障碍和胰岛素抵抗似乎是这种关系的一些关键因素,因为胰岛素的主要作用靶点是骨骼肌。本综述旨在全面讨论这些疾病所涉及的主要代谢和生理途径。MAFLD和肌肉减少症通过一个复杂的病理生理机制网络相互关联,如胰岛素抵抗、骨骼肌组织生成能力、慢性炎症状态、氧化应激和线粒体功能障碍,这些是这种关系的主要促成因素。此外,在一项临床分析中,与仅患有MAFLD的患者相比,患有肌肉减少症和MAFLD的患者表现出更严重的肝纤维化。这些同时患有这两种疾病的患者在接受肌肉减少症治疗后,其MAFLD也出现了临床改善,这进一步加强了它们之间的关联。生活方式的改变以及饮食治疗和增加体育活动等非药物干预措施无疑会改善这种情况。