Obesity is a concern for bone health with aging

Abstract

Accumulating evidence supports a complex relationship between adiposity and osteoporosis in overweight/obese individuals, with local interactions and endocrine regulation by adipose tissue on bone metabolism and fracture risk in elderly populations. This review was conducted to summarize existing evidence to test the hypothesis that obesity is a risk factor for bone health in aging individuals. Mechanisms by which obesity adversely affects bone health are believed to be multiple, such as an alteration of bone-regulating hormones, inflammation, oxidative stress, the endocannabinoid system, that affect bone cell metabolism are discussed. In addition, evidence on the effect of fat mass and distribution on bone mass and quality is reviewed together with findings relating energy and fat intake with bone health. In summary, studies indicate that the positive effects of body weight on bone mineral density cannot counteract the detrimental effects of obesity on bone quality. However, the exact mechanism underlying bone deterioration in the obese is not clear yet and further research is required to elucidate the effect of adipose depots on bone and fracture risk in the obese population.

Dual Targeting of Bile Acid Receptor-1 (TGR5) and Farnesoid X Receptor (FXR) Prevents Estrogen-Dependent Bone Loss in Mice

“…Osteoclasts are multinucleated giant cells derived from hematopoietic progenitor cells and are mitochondria‐rich cells with a high energy demand . Consequently, osteoporosis, like obesity and diabetes, could be another disorder of energy metabolism …”

Effects of dietary fatty acid content on humeral cartilage and bone structure in a mouse model of diet‐induced obesity

“…This risk has been partially attributed to a decrease in mineral content, but the relationship between obesity and BMD is incompletely understood. Some clinical studies indicate a positive relationship between body mass index (BMI) and BMD, but others show the opposite or no change . Similarly, animal models of obesity show varying bone responses to obesity, with some studies showing an increase in bone formation and others a decrease .…”

“…Adiponectin, acting through FoxO1, has been shown in some situations to decrease osteoblast proliferation and promote apoptosis . Under what conditions ω‐3 PUFAs result in catabolic or anabolic affects is still an active area of research, with many studies reporting protective effects of ω‐3 PUFA supplementation on bone . Although awareness of ω‐3 PUFA benefits is increasing, the average American diet has proportionally more ω‐6 PUFAs and saturated fats .…”

Transdifferentiation of adipocytes to osteoblasts: potential for orthopaedic treatment

“…[19] As this epidemic continues to grow, there is an increasing body of evidence that contradicts the initial belief that a greater body mass has positive effects for bone health. [6] Multiple mechanisms have been implicated such as the low grade inflammation that often accompanies obesity, a change in hormones that normally regulates bone homoeostasis, increased levels of oxidative stress and the shift in bone cell metabolism. [6] Obesity is associated with a change in cytokine profile as implicated by the increase in circulating pro-inflammatory cytokines such as the tumour necrosis factor-a (TNF-a),interleukin-6 (IL-6), monocyte chemoattractant protein-1 and C-reactive protein (CRP).…”

“…[6] Multiple mechanisms have been implicated such as the low grade inflammation that often accompanies obesity, a change in hormones that normally regulates bone homoeostasis, increased levels of oxidative stress and the shift in bone cell metabolism. [6] Obesity is associated with a change in cytokine profile as implicated by the increase in circulating pro-inflammatory cytokines such as the tumour necrosis factor-a (TNF-a),interleukin-6 (IL-6), monocyte chemoattractant protein-1 and C-reactive protein (CRP). [18,20] These pro-inflammatory mediators act as key players in osteoclast differentiation via regulation of the RANKL/RANK/OPG signalling pathway: RANKL is a bone resorption marker and osteoclast cytokine, RANK is the receptor that RANKL binds to for initiation of osteoclast differentiation, whereas OPG acts as a decoy receptor that prevents the RANKL-RANK complex from forming and thereby regulating the function of RANKL.…”