Aging, obese-insulin resistance, and bone remodeling.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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