School of Health, Medical and Applied Sciences, Central Queensland University, Rockhampton, Queensland, Australia, 4702; Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, University of Queensland St Lucia, Brisbane, Queensland, Australia, 4072.
School of Health, Medical and Applied Sciences, Central Queensland University, Rockhampton, Queensland, Australia, 4702.
Diabetes Metab Syndr. 2020 Sep-Oct;14(5):867-875. doi: 10.1016/j.dsx.2020.06.006. Epub 2020 Jun 9.
Metabolic syndrome is the concurrent presentation of multiple cardiovascular risk factors, including obesity, insulin resistance, hyperglycemia, dyslipidemia and hypertension. It has been suggested that some of these risk factors can have detrimental effects on the skeletal muscle while others can be a direct result of skeletal muscle abnormalities, showing a two-way directionality in the pathogenesis of the condition. This review aims to explore this bidirectional correlation by discussing the impact of metabolic syndrome on skeletal muscle tissue in general and will also discuss ways in which skeletal muscle alterations may contribute to the pathogenesis of metabolic syndrome.
Literature searches were conducted with key words (e.g. metabolic syndrome, skeletal muscle, hyperglycemia) using PubMed, EBSCOhost, Science Direct and Google Scholar. All article types were included in the search.
The pathological mechanisms associated with metabolic syndrome, such as hyperglycemia and inflammation, have been associated with changes in skeletal muscle fiber composition, metabolism, insulin sensitivity, mitochondrial function, and strength. Additionally, some skeletal muscle alterations, particularly mitochondrial dysfunction and insulin resistance, are suggested to contribute to the development of metabolic syndrome. For example, the suggested underlying mechanisms of sarcopenia development are also contributors to metabolic syndrome pathogenesis.
Whilst numerous studies have identified a relationship between metabolic syndrome and skeletal muscle abnormalities, further investigation into the underlying mechanisms is needed to elucidate the best prevention and management strategies for these conditions.
代谢综合征是多种心血管危险因素的同时表现，包括肥胖、胰岛素抵抗、高血糖、血脂异常和高血压。有人认为，这些危险因素中的一些可能对骨骼肌产生不利影响，而另一些则可能是骨骼肌异常的直接结果，表明该疾病的发病机制具有双向方向性。本综述旨在通过讨论代谢综合征对骨骼肌组织的总体影响来探讨这种双向相关性，并讨论骨骼肌改变如何可能有助于代谢综合征的发病机制。
使用 PubMed、EBSCOhost、Science Direct 和 Google Scholar 等关键词（例如代谢综合征、骨骼肌、高血糖）进行文献检索。搜索中包括所有类型的文章。
与代谢综合征相关的病理机制，如高血糖和炎症，与骨骼肌纤维组成、代谢、胰岛素敏感性、线粒体功能和强度的变化有关。此外，一些骨骼肌改变，特别是线粒体功能障碍和胰岛素抵抗，被认为有助于代谢综合征的发展。例如，肌少症发展的潜在机制也可能是代谢综合征发病机制的促成因素。
虽然许多研究已经确定了代谢综合征与骨骼肌异常之间的关系，但需要进一步研究潜在机制，以阐明这些疾病的最佳预防和管理策略。
