Endocrine Abstracts

Background: Bone mass is low and fracture risk is higher in obese children. We wished to ascertain the relationships of obesity-related changes in hormones with skeletal microstructure.

Method: Children aged 8–15 years matched by gender and pubertal stage were recruited into lean and obese groups (18 pairs). We used high resolution peripheral quantitative computed tomography (HRpQCT – resolution-82 μm) to assess three-dimensional cortical and trabecular microstructure at load-bearing and non-load bearing sites. Lean and fat mass percentage (%) were measured by DXA. Leptin, adiponectin, testosterone and oestrogen were measured by immunoassay.

Results: Lean and obese children were 12.9±2.0 years and 12.6±1.9 years (P=0.23) respectively. There was no difference in height SDS between groups. Radial cortical porosity (mean difference −0.01 (95% CI: −0.02, −0.004), P=0.004) and cortical pore diameter (mean difference −0.005 mm (95% CI: −0.009, −0.001), P=0.009) were lower in obese children. Tibial trabecular thickness was lower (mean difference −0.009 mm (95% CI: −0.015, −0.004), P=0.002) and trabecular number was higher (mean difference 0.23/mm (95% CI: 0.08, 0.38), P=0.006) in obese children. At the radius, fat mass % negatively correlated cortical porosity (r=0.57, P<0.001) and cortical pore diameter (r=0.38, P=0.02) and negatively correlated with tibial trabecular thickness (r=−0.62, P<0.001).

Leptin was higher in obese children (805.3±440.6 vs 98.1±75.4, P<0.001) and was inversely related to radial cortical porosity (r=0.60, 95% CI: (−0.80, −0.30), P<0.001), mean radial cortical pore diameter (r=0.51, 95% CI (−0.75, −0.16), P=0.002), and tibial trabecular thickness (r=0.55, 95%CI: (−0.78, −0.21), P=0.001). In multivariate analyses that included all measured hormones, leptin remained inversely correlated to radial cortical porosity (r²=0.48, P=0.002), mean radial cortical pore diameter (r²=0.26, P=0.01) and tibial trabecular thickness (r²=0.22, P=0.02).

Conclusion: Childhood obesity improves radial cortical porosity but negatively impacts on tibial trabecular microstructure. Leptin appears to be a key hormone mediating these changes. Maladaption of tibial trabecular microstructure may result in an increased risk of tibial fracture in obese children.