The contribution of insulin resistance vs. adiposity in determining bone mineral density (BMD), bone turnover and fracture risk in humans remains unclear. Bone mineral density (BMD) predicts fracture risk, and obesity is associated with higher BMD. People with both type 1 and type 2 diabetes have increased fracture risk, despite many people with type 2 diabetes being overweight or obese, with normal BMD. Factors that contribute to increased fracture risk in diabetes are insulin use, increased risk of falls due to neuropathy and retinopathy, inflammation, glycation of collagen, use of PPAR-y agonists and poor bone quality related to poor nutrition. Fracture risk in diabetes does not appear to be associated with BMD, and so must occur at a cellular level.
Bone turnover markers are lower in people with the metabolic syndrome, and in diabetes, and is associated with insulin resistance rather than adiposity.
This talk will review published data looking at fracture rates and bone turnover marker levels in people with obesity, insulin resistance and diabetes. Data will be presented from studies looking at bone turnover markers performed locally. These data suggest that increased visceral adiposity and higher fasting insulin levels in insulin-resistant states is associated with lower fasting OC and CTx, and failure to further suppress with more insulin. This raises the possibility that diabetic osteopathy may be considered another complication of diabetes.