AGE Research Group, Newcastle University Institute for Translational and Clinical Research, Newcastle Upon Tyne, UK.
NIHR Newcastle Biomedical Research Centre, Newcastle University, Newcastle upon Tyne NHS Foundation Trust and Cumbria, Northumberland and Tyne and Wear NHS Foundation Trust, Newcastle Upon Tyne, UK.
Drugs Aging. 2023 Aug;40(8):703-719. doi: 10.1007/s40266-023-01042-4. Epub 2023 Jul 24.
Sarcopenia, the age-related loss of muscle strength and mass or quality, is a common condition with major adverse consequences. Although the pathophysiology is incompletely understood, there are common mechanisms between sarcopenia and the phenomenon of accelerated ageing seen in diabetes mellitus. Drugs currently used to treat type 2 diabetes mellitus may have mechanisms of action that are relevant to the prevention and treatment of sarcopenia, for those with type 2 diabetes and those without diabetes. This review summarises shared pathophysiology between sarcopenia and diabetes mellitus, including the effects of advanced glycation end products, mitochondrial dysfunction, chronic inflammation and changes to the insulin signalling pathway. Cellular and animal models have generated intriguing, albeit mixed, evidence that supports possible beneficial effects on skeletal muscle function for some classes of drugs used to treat diabetes, including metformin and SGLT2 inhibitors. Most human observational and intervention evidence for the effects of these drugs has been derived from populations with type 2 diabetes mellitus, and there is a need for intervention studies for older people with, and at risk of, sarcopenia to further investigate the balance of benefit and risk in these target populations. Not all diabetes treatments will be safe to use in those without diabetes because of variable side effects across classes. However, some agents [including glucagon-like peptide (GLP)-1 receptor agonists and SGLT2 inhibitors] have already demonstrated benefits in populations without diabetes, and it is these agents, along with metformin, that hold out the most promise for further investigation in sarcopenia.
肌肉减少症是一种与年龄相关的肌肉力量和质量或身体成分损失的病症，是一种常见病症，会带来严重的不良后果。尽管其病理生理学尚未完全清楚，但肌肉减少症和糖尿病中加速衰老的现象之间存在共同的机制。目前用于治疗 2 型糖尿病的药物可能具有与预防和治疗 2 型糖尿病和非糖尿病患者的肌肉减少症相关的作用机制。这篇综述总结了肌肉减少症和糖尿病之间的共同病理生理学，包括晚期糖基化终产物、线粒体功能障碍、慢性炎症和胰岛素信号通路变化的影响。细胞和动物模型产生了有趣的、尽管混杂的证据，支持某些用于治疗糖尿病的药物类别对骨骼肌功能可能有有益的影响，包括二甲双胍和 SGLT2 抑制剂。这些药物对这些人群的影响的大多数人体观察性和干预性证据都来自 2 型糖尿病患者，需要对患有肌肉减少症和有肌肉减少症风险的老年人进行干预研究，以进一步研究这些目标人群的获益和风险平衡。并非所有糖尿病治疗方法对无糖尿病的人都是安全的，因为不同类别的药物有不同的副作用。然而，一些药物[包括胰高血糖素样肽 (GLP)-1 受体激动剂和 SGLT2 抑制剂]已经在无糖尿病的人群中显示出益处，这些药物以及二甲双胍，为进一步研究肌肉减少症提供了最大的希望。
