No effect of copper supplementation on biochemical markers of bone metabolism in healthy young adult females despite apparently improved copper status

Objective: To investigate the effects of increasing Cu intakes, above the usual dietary intake, on biomarkers of bone metabolism in healthy young adult females (aged 21-28y) over a 4 week period. Design: A double-blind, placebo-controlled randomised repeat crossover Cu supplementation trial. Setting: The study was conducted at the Royal Veterinary and Agricultural University (RVAU), Copenhagen, Denmark. Subjects: Sixteen healthy young adult females aged 20-28 y were recruited from among students at the RVAU. Intervention: During the 4 week intervention periods in this randomised, crossover trial (3x4 weeks with a minimum 3 week wash-out period), each subject received, in addition to their usual diet, either 3 or 6 mg elemental Cu/day as CuS[O.sub.4] or a matching placebo. On the last 3 days of each dietary period 24h urines were collected. In addition, blood was collected on the last day of each dietary period. Results: Serum Cu and erythrocyte superoxide dismutase (but not caeruloplasmin protein concentration or activity (putative indices of Cu status)) were significantly increased (P < 0.05) after daily Cu supplementation with 3 and 6 mg/day for 4 weeks. Serum osteocalcin (biomarker of bone formation), urinary creatinine (Cr) concentration, urinary pyridinoline (Pyr)/Cr or deoxypyridinoline (Dpyr)/Cr excretion, or daily urinary Pyr or Dpyr excretion (biomarkers of bone resorption) were unaffected by Cu supplementation. Conclusion: Copper supplementation of the usual diet in healthy young adult females, while apparently improving Cu status, had no effect on biochemical markers of bone formation or bone resorption over 4 week periods. Sponsorship: Funding from the European Commission. Descriptors: copper status; bone; biomarkers; young adult females
Introduction Copper has an important role in the metabolism of the skeleton, where it performs a key catalytic function as a cofactor for lysyl oxidase (E.C. 1.4.3.13), a Cu-dependent extracellular [...]