We investigated the effect of bone turnover on
glucose homeostasis, fat distribution and
adipokine production during anabolic treatment with PTH. This is a parallel, randomized controlled, open label, trial. The randomization was done by computer generated tables to allocate treatments. Forty-six postmenopausal osteoporotic non-diabetic women were assigned to treatment with
calcium and colecalcipherol with (24) or without (22)
PTH 1-84. Patients were recalled after 3, 6, 12 and 18 months of treatment and markers of bone turnover,
glucose metabolism,
adipokine secretion and fat distribution were analyzed. Markers of bone turnover and
adipokines were measured by ELISA.
Glucose metabolism was evaluated by an oral
glucose load test and
insulin resistance and secretion were calculated. Fat and lean mass were evaluated by anthropometric measures. The effect of treatment on measured variables was analyzed by repeated measure test, and its effect on
glucose was also evaluated by mediation analysis after correction for possible confounders. Twenty patients in the
calcium and
vitamin D groups and 19 in the group treated with
PTH 1-84 completed the study. There were no significance adverse events. Treatment with PTH increases
osteocalcin, both total (OC) and undercarboxylated (uOC), and decreases
blood glucose, without influence on insulin secretion, resistance and pancreatic β cell function. Treatment with PTH does not influence fat distribution and
adipokine production. The results of the mediation analyses suggest a total effect of PTH on
blood glucose, moderately mediated by OC and to a less extent by uOC. Here we suggest that treatment with PTH influences
glucose metabolism partially through its effect on bone turnover, without influence on insulin secretion, resistance, pancreatic β cell function and fat mass.