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A cross‐sectional study of osteocalcin and body fat measures among obese adolescents
Author(s) -
Lenders Carine M.,
Lee Phillip D.K.,
Feldman Henry A.,
Wilson Darrell M.,
Abrams Stephanie H.,
Gitelman Stephen E.,
Klish William J.,
Wertz Marcia S.,
Taylor George A.,
Alongi Richard T.,
Chen Tai C.,
Holick Michael F.
Publication year - 2013
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20131
Subject(s) - endocrinology , osteocalcin , medicine , leptin , parathyroid hormone , vitamin d and neurology , obesity , body mass index , vitamin d deficiency , adipose tissue , overweight , chemistry , alkaline phosphatase , calcium , biochemistry , enzyme
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 mm 2 ) 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 mm 2 , 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.