title: Vitamin D binding protein, bone status and body composition in community-dwelling elderly men.
abstract: The vitamin D binding protein (DBP) is the major carrier protein for vitamin D metabolites in plasma. Polymorphisms in DBP have been described to be associated with an increased bone fracture risk and diabetes. The present study investigates the influence of both phenotypic and (TAAA)(n)-Alu repeat DBP-polymorphism and DBP-concentration on bone mineral density, body composition, bone turnover- and metabolic markers in a cohort of ambulatory elderly men. We included 211 men (>70 years) in this study. Bone mineral density (BMD) was determined by dual energy X-ray absorptiometry. Bone turnover was assessed by measurement of serum osteocalcin, serum and urinary C-terminal telopeptides of type I collagen and urinary deoxypyridinoline, together with 25(OH)-vitamin D and 1,25(OH)(2)-vitamin D concentrations. DBP-phenotypes were determined electrophoretically and the (TAAA)(n)-Alu repeat polymorphism was determined by polymerase chain reaction. Body composition was estimated using bioelectrical impedance analysis, together with handgrip and arm strength, fasting serum glucose and leptin concentrations. No differences in BMD or bone turnover markers among DBP-phenotypes or (TAAA)(n)-genotypes were observed in this study. Serum 25(OH)-vitamin D was comparable among DBP-variants and did not relate to DBP-concentrations, whereas 1,25(OH)(2)-vitamin D was different among DBP-phenotypes and was correlated positively with DBP-concentrations. DBP-concentrations related positively to body mass index, fat mass, leptin and glucose concentration. The correlation with leptin remained significant after correction for fat mass. Fasting glucose concentrations were different among DBP-phenotypes, whereas no difference was observed between (TAAA)(n)-genotypes. In conclusion, serum 1,25(OH)(2)-vitamin D concentrations are codetermined by DBP-phenotypes and DBP-concentrations. No major effect of DBP-polymorphism was demonstrated on BMD, bone turnover markers or body composition.
authors.affiliation: Laboratory of Clinical Chemistry, Microbiology and Immunology 2P8, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium. Youri.Taes@UGent.be
authors.forename: Youri E C
authors.initials: YE
authors.lastname: Taes
authors.forename: Stefan
authors.initials: S
authors.lastname: Goemaere
authors.forename: Guangming
authors.initials: G
authors.lastname: Huang
authors.forename: Inge
authors.initials: I
authors.lastname: Van Pottelbergh
authors.forename: Dirk
authors.initials: D
authors.lastname: De Bacquer
authors.forename: Bruno
authors.initials: B
authors.lastname: Verhasselt
authors.forename: Celine
authors.initials: C
authors.lastname: Van den Broeke
authors.forename: Joris R
authors.initials: JR
authors.lastname: Delanghe
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Kaufman
mesh_terms: D015502:Absorptiometry, Photon; D000368:Aged; D020087:Alu Elements / Q000235:genetics; D015415:Biomarkers / Q000097:blood / Q000378:metabolism / Q000652:urine; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition / Q000235:genetics*; D015519:Bone Density / Q000235:genetics*; D016723:Bone Remodeling / Q000235:genetics*; D001842:Bone and Bones / Q000000981:diagnostic imaging / Q000378:metabolism; D024042:Collagen Type I / Q000097:blood / Q000652:urine; D017097:Electric Impedance; D006801:Humans; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010455:Peptides / Q000097:blood / Q000652:urine; D011110:Polymorphism, Genetic; D014807:Vitamin D / Q000097:blood / Q000378:metabolism / Q000652:urine; D014809:Vitamin D-Binding Protein / Q000097:blood / Q000235:genetics*
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D024042:Collagen Type I; D020738:Leptin; D010455:Peptides; D014809:Vitamin D-Binding Protein; C052929:collagen type I trimeric cross-linked peptide; D015675:Osteocalcin; D014807:Vitamin D