In the recent years the role of the skeleton in glucose and energy homeostasis has been studied. In particular the osteoblast-specific protein osteocalcin (OC), in its undercarboxylated form (uOC) has been shown to influence glucose homeostasis in animal models.
The aim of our study is to evaluate if the intermittent administration of 184 PTH could influence glucose metabolism through its anabolic action on the skeleton.
We enrolled in the study 43 women affected by postmenopausal osteoporosis; the patients were randomly assigned to treatment with:
i) 1-84 PTH 100 μg plus calcium 1200 mg and vitamin D 800 UI daily (21).
ii) calcium 1200 mg and vitamin D 800 UI daily (22).
Glucose and bone metabolism were evaluated at basal and after 3, 6, 12 and 18 months of treatment. Glucose metabolism was evaluated trough an oral glucose tolerance test with 75 g of glucose and blood sampling for glucose and insulin at 0′, 30′, 60′, 90′, and 120′. OC, uOC, adiponectin, and leptin were measured at each visit by ELISA technique. Body fat was measured by plicometry at each visit.
In PTH treated patients fasting plasma glucose significantly decreases during therapy, without increase in insulin secretion. The treatment with PTH increases the production of uOC, and this increase is inversely correlated with fasting plasma glucose, whereas there is no effect of treatment on fat distribution or adipokines secretion.
Our data demonstrated that treatment with intermittent PTH lowers plasma glucose metabolism and suggest that this effect is mediated by the increase in uOC.
17 May 2014 - 20 May 2014