MedWire News: The relationship between Type 2 diabetes and fracture risk may be due to the inhibition of cortical bone development by insulin, the results of a peripheral quantitative computed tomography (pQCT) study suggest.
Although dual-energy X-ray absorptiometry-measured bone mineral density (BMD) is inversely associated with fracture risk, the presence of Type 2 diabetes alters this relationship, with patients carrying an increased risk for nonvertebral fracture despite elevated lumbar spine and femoral neck BMD, explain Jon Tobias (University of Bristol, UK) and co-workers.
To investigate further, the team collated data from the Avon Longitudinal Study of Parents and Children on fasting insulin, obesity, and pQCT measurements of the mid-tibia for 2784 boys and girls aged an average of 15.5 years.
"One of the limitations in dissecting out relationships between insulin resistance, [bone mineral content] BMC, and fat deposition is the difficulty in adjusting for body size and stature, particularly in children where differences are exaggerated by variation in age and maturational status," the researchers explain.
"pQCT overcomes this limitation by enabling effects on bone size to be distinguished from those on other parameters such as cortical bone density and the amount of trabecular bone."
Analysis revealed a significant negative association between insulin and cortical BMD after adjustment for age. This continued to be significant after further adjustment for height, muscle cross-sectional area (MCSA), subcutaneous fat, and muscle density.
Insulin was significantly and positively associated with periosteal circumference (PC) after taking into consideration age, but the association was inverse when height and body composition were considered.
In addition, there were negative correlations between insulin and PC both directly and via muscle density - a marker for intramuscular fat - and positive associations between insulin and PC via subcutaneous fat and MCSA.
"We found an inverse relationship between insulin and PC via intramuscular fat, suggesting a lipotoxic effect on bone," Tobias et al write in the Journal of Bone and Mineral Research.
"However, an inverse association between insulin and both PC and [cortical BMD] persisted after adjusting for all body composition variables, suggesting insulin also acts to inhibit bone development via additional pathways yet to be elucidated," they continue.
The team recommends further research into this mechanism, noting that "any tendency for insulin to impair cortical bone development may have important clinical consequences, such as contributing to the excess in fracture risk observed in conditions associated with hyperinsulinemia such as type 2 diabetes mellitus."
MedWire (www.medwire-news.md) is an independent clinical news service provided by Springer Healthcare Limited. © Springer Healthcare Ltd; 2012