Bone Abstracts (2013) 2 P40 | DOI: 10.1530/boneabs.2.P40

Altered bone metabolism in obese children: the pathogenic role of adipocytokines and inflammation

Pawel Abramowicz, Jerzy Konstantynowicz, Irena Werpachowska, Jacek Jamiolkowski, Maciej Kaczmarski & Janina Piotrowska-Jastrzebska


Medical University of Bialystok, Bialystok, Poland. *Winner of New Investigator Award


Objective: Associations between childhood obesity and disturbed bone metabolism have been extensively studied. Both RANK/RANKL/OPG and adipocytokines are involved in bone metabolism in obese individuals although published data remain inconsistent. Some reports show evidence of protective role of adiposity in the maintenance of skeletal mass, whereas others fail to support this evidence or even demonstrate an increased fragility. The aim of the study was to assess bone metabolism in obese children and to evaluate influence of adipocytokines on their bone mass.

Methods: In 40 obese children aged 7.1–17.6 years and 30 non-obese controls, total and lumbar spine bone mineral content (BMC) and density (BMD) were determined using dual-energy X-ray absorptiometry (DXA). Serum lipids, total calcium (Catotal), 25-hydroxycholecalciferol (25OHD), parathormone (PTH), leptin, adiponectin, osteocalcin (OC), osteoprotegerin (OPG), RANK-ligand (RANKL), and high-sensitivity CRP (hsCRP) were measured.

Results: Higher levels of leptin (P<0.001), hsCRP (P<0.001), Catotal (P=0.012), PTH (P<0.001) were found in obese children. Serum adiponectin and OC were lower in obese individuals (P=0.005 and P=0.12 respectively). Total and spine BMD and BMC were higher in the obese than in controls. We found association between adiposity and hsCRP which correlated with leptin (r=0.55; P<0.001), RANKL (r=0.25; P=0.04), PTH (r=0.36; P=0.004), and total cholesterol and triglycerides (r=0.38, 0.39; both P=0.001). Furthermore, PTH activity correlated positively with leptin and inversely with adiponectin levels. There was no difference in RANK/RANKL/OPG pathway activity between obese and controls, and no correlations were found between its activity and adipocytokines levels either. No differences were found in concentration of 25OHD between the groups.

Conclusions: These results support the role of inflammation in obesity. Chronic inflammation with altered adipocytokine levels may be responsible for inadequate bone metabolism in childhood obesity. Higher PTH and Catotal concentrations may reflect parathyroid hyperactivity as a mechanism leading to bone resorption in obese individuals despite excessive BMD accrual. Coincidence of hypercalcemia and decreased adiponectin seems an additional risk factor of atherosclerosis during growth. More research is needed to understand the role of PTH in bone and fat relationships in children.

The study was supported by the Human Capital Programme (8.2.1.) organized by the European Social Fund (EU Structural Fund).

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