CONTEXT: Undercarboxylated osteocalcin (ucOC) has been shown to affect glucose metabolism in mice. We recently randomized patients with hypoparathyroidism to treatment with PTH or placebo and demonstrated a marked increase in total osteocalcin. OBJECTIVE: To investigate whether there was a similar increase in ucOC and whether that increase affected glucose metabolism. DESIGN: A 24-week randomized, placebo-controlled trial. SETTING:Ambulatory patients in a research facility. PATIENTS: Sixty-two patients aged 31-78 years with hypoparathyroidism, of which 58 completed the trial. INTERVENTION: 100 μg/d of PTH (1-84). MAIN OUTCOME MEASURE: Change in ucOC. RESULTS:ucOC increased by 1185.0 ± 814.4% (mean ± SD) 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 = .04). Glucose, adiponectin, leptin, homeostasis model of assessment for insulin resistance, total body fat mass, or truncal fat did not change significantly. In addition, the number of hypercalcemic episodes per patient was 3.7 ± 2.9 (mean ± SD) in the PTH-treated group but only 0.2 ± 0.6 in the placebo group (P < .001). Moreover, there was a significant and negative correlation between the change in ucOC and change in body weight (P = .004) or change in total body fat mass (P = .03), and a negative but nonsignificant correlation between the number of hypercalcemic episodes and percentage change in body weight (r = -0.32; P = .1). Change in ucOC did not significantly correlate with changes in other parameters. CONCLUSIONS: An explanation for the weight loss may be subtle hypercalcemia in PTH treatment inhibiting appetite. Our data do not support a role for ucOC in energy metabolism in humans.
RCT Entities:
CONTEXT: Undercarboxylated osteocalcin (ucOC) has been shown to affect glucose metabolism in mice. We recently randomized patients with hypoparathyroidism to treatment with PTH or placebo and demonstrated a marked increase in total osteocalcin. OBJECTIVE: To investigate whether there was a similar increase in ucOC and whether that increase affected glucose metabolism. DESIGN: A 24-week randomized, placebo-controlled trial. SETTING: Ambulatory patients in a research facility. PATIENTS: Sixty-two patients aged 31-78 years with hypoparathyroidism, of which 58 completed the trial. INTERVENTION: 100 μg/d of PTH (1-84). MAIN OUTCOME MEASURE: Change in ucOC. RESULTS: ucOC increased by 1185.0 ± 814.4% (mean ± SD) 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 = .04). Glucose, adiponectin, leptin, homeostasis model of assessment for insulin resistance, total body fat mass, or truncal fat did not change significantly. In addition, the number of hypercalcemic episodes per patient was 3.7 ± 2.9 (mean ± SD) in the PTH-treated group but only 0.2 ± 0.6 in the placebo group (P < .001). Moreover, there was a significant and negative correlation between the change in ucOC and change in body weight (P = .004) or change in total body fat mass (P = .03), and a negative but nonsignificant correlation between the number of hypercalcemic episodes and percentage change in body weight (r = -0.32; P = .1). Change in ucOC did not significantly correlate with changes in other parameters. CONCLUSIONS: An explanation for the weight loss may be subtle hypercalcemia in PTH treatment inhibiting appetite. Our data do not support a role for ucOC in energy metabolism in humans.