Aging, obese-insulin resistance, and bone remodeling.

Mech Ageing Dev

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 Biology and Diagnostic Sciences, Faculty of Dentistry, Chiang Mai University, Chiang Mai, 50200, Thailand. Electronic address:

Published: October 2020

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.

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http://dx.doi.org/10.1016/j.mad.2020.111335DOI Listing

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