Osteocalcin (OC) is produced by osteoblasts in an undercarboxylated form (ucOC). Recently ucOC has been shown to influence energy metabolism in mice. In hypoparathyroidism (HPT) secretion of parathyroid hormone (PTH) is decreased or absent suppressing bone turnover. We recently randomised patients with HPT to treatment with PTH or placebo and demonstrated a marked increase in bone turnover. In particular, OC increased by more than 800%. We therefore investigated in the same cohort if there was a similar increase in ucOC and if that increase affected energy metabolism. 62 patients with HPT were randomised to treatment with either 100 μg PTH1-84 (Preotact®, Nycomed, Denmark) or placebo for 24 weeks. We measured fat mass using DXA at baseline and after 24 weeks. We took fasting blood samples at baseline and after 24 weeks. Fasting plasma glucose was measured using standard techniques and. By using ELISA we determined ucOC, leptin, adiponectin, and insulin. As a measure of insulin resistance we calculated HOMA-IR. During treatment ucOC increased by 1185.0±814.4% in the PTH treated group and by 69.3±79.4% in the placebo group (p<10−50). In addition, body weight decreased by 1.1±4.0% in the treatment group and increased 0.8±2.5% in the placebo group (p=0.04). Glucose, adiponectin, leptin, HOMA-IR, total body fat mass, or truncal fat did not change significantly. Moreover, there was a significant and negative correlation between change in ucOC and change in body weight (p=0.004) or change in total body fat mass (p=0.03). Change in ucOC did not significantly correlate with changes in other parameters. In conclusion PTH treatment significantly increased ucOC and decreased body weight, however, insulin resistance or adipokines were unaffected. An explanation for the weight loos may be subtle hypercalcaemia in PTH treatment inhibiting appetite. Our data do not support a role for ucOC in energy metabolism in humans.
Disclosure: The authors declared no competing interests. This work was supported by a grant from the Torben and Alice Frimodt Foundation.