A cross‐sectional study of osteocalcin and body fat measures among obese adolescents |
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Authors: | Carine M Lenders Phillip DK Lee Henry A Feldman Darrell M Wilson Stephanie H Abrams Stephen E Gitelman William J Klish Marcia S Wertz George A Taylor Richard T Alongi Tai C Chen Michael F Holick |
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Institution: | 1. Boston Medical Center, Boston University School of Medicine;2. Children's Hospital Boston, Harvard Medical School;3. Mattel Children's Hospital, David Geffen School of Medicine at UCLA, Los Angeles;4. Lucile S. Packard Children's Hospital, Stanford University School of Medicine;5. Elisabeth Glaser Pediatric Research Network Obesity Study Group;6. Children's Medical Center, University of California, San Francisco;7. Texas Children's Hospital, Baylor College of Medicine |
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Abstract: | Osteocalcin (OCN), a marker of osteoblast activity, has been implicated in the regulation of energy metabolism by the skeleton and thus may affect body fat measures. Objective: To examine the relationships of OCN to body fat measures and whether they vary according to markers of energy and vitamin D metabolism. Design and Methods: Data were obtained from 58 obese adolescents aged 13‐17.9 years (38 females, 8 black or African‐American). Total fat mass (FM) dual X‐ray absorptiometry (DXA)] and visceral adipose tissue (VAT) computerized axial tomography (CT)] were calculated. Blood tests included leptin, OCN, 25‐hydroxyvitamin D 25(OH)D], parathyroid hormone (PTH), thyroid function tests, and triglycerides. Markers of glucose metabolism were obtained from fasting and OGTT samples. Results and Conclusions: Adolescents with 25(OH)D <20 ng mL?1 were considered deficient (n = 17/58); none had high PTH (PTH ≥ 65 pg mL?1). OCN was associated with lower VAT (?84.27 ± 33.89 mm2) and BMI (?0.10 ± 0.05 kg m?2), not FM (P = 0.597) in a core model including age, sex, race, geographic latitude, summer, height z‐score, and tanner stage. Adding 25(OH)D deficiency and PTH attenuated the inverse association of OCN to VAT. There was a significant interaction of OCN and 25(OH)D deficiency on FM (0.37 ± 0.18 kg, P = 0.041) and BMI (0.28 ± 0.10 kg m?2, P = 0.007) in this adjusted model, which was further explained by leptin. Adding A1C to the core model modified the relationship of OCN to VAT (?93.08 ± 35.05 mm2, P = 0.011), which was further explained by HOMA‐IR. In summary, these findings provide initial evidence for a relationship between OCN and body fat measures that is dependent on energy metabolism and vitamin D status among obese adolescents. |
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