Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand; Department of Oral Surgery, Faculty of Dentistry, Chiang Mai University, Chiang Mai, 50200, Thailand.
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand; Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Mech Ageing Dev. 2020 Oct;191:111335. doi: 10.1016/j.mad.2020.111335. Epub 2020 Aug 25.
Aging, obesity, and insulin resistance are known to cause the impairment of bone regulation, resulting in an imbalance in bone homeostasis and pathological bone. The natural deterioration associated with the aging process, including increased adipogenicity, menopause, andropause and alteration of mesenchymal stem cell fate have been shown to be potential causes of decreased bone density, resulting in osteoporosis, in which is a major risk factor of bone fracture in elderly people. Furthermore, functional limitations of the aging musculoskeletal system cause physical inactivity and increased adipogenicity. Therefore obesity in aged population has been dramatically observed. Several evidence demonstrated that obesity in aged individual leads to the acceleration and aggravation of unfavorable effects to general health, particularly the deterioration of bone health, including reduction in bone formation, increased bone resorption, greater adipose tissue accumulation, impaired bone architecture, and bone fragility. Therefore, the present review aimed to summarize and discuss the effects of aging, obesity, and aging with obesity on bone remodeling. The possible mechanistic insights of bone homeostasis and the interventions for the improvement of bone quality in aged and obese individuals have been included and discussed.
衰老是导致骨调节受损的已知原因,肥胖和胰岛素抵抗会导致骨调节受损,从而导致骨内稳态失衡和病理性骨。与衰老过程相关的自然恶化,包括脂肪生成增加、绝经、更年期和间充质干细胞命运改变,已被证明是骨密度降低导致骨质疏松症的潜在原因,骨质疏松症是老年人骨折的主要危险因素。此外,衰老的肌肉骨骼系统的功能限制导致身体活动减少和脂肪生成增加。因此,在老年人群中观察到肥胖的急剧增加。有几项证据表明,肥胖会加速和加重对整体健康的不利影响,特别是对骨骼健康的恶化,包括骨形成减少、骨吸收增加、更多的脂肪组织堆积、骨结构受损和骨脆性增加。因此,本综述旨在总结和讨论衰老、肥胖以及衰老与肥胖对骨重塑的影响。讨论了骨内稳态的可能机制见解以及改善肥胖和老年人骨质量的干预措施。