Effect of exogenous intermittent recombinant human PTH 1-34 administration and chronic endogenous parathyroid hormone excess on glucose homeostasis and insulin sensitivity.

We aimed to evaluate the effects of exogenous intermittent teriparatide (rhPTH 1-34) administration versus the chronic exposure to excess endogenous parathyroid hormone (PTH), as in pHPT, on glucose homeostasis. Two patient groups were studied: Group 1 included 25 normocalcemic women with postmenopausal osteoporosis (age 65.2+/-1.6 years) studied before and six months after teriparatide initiation; Group 2 included 19 postmenopausal women with pHPT (age 55.2+/-2.5 years) studied before and six months after successful parathyroidectomy. Calcium - total (Ca) and corrected (CCa) - ALP, PTH, as well as glucose and insulin concentrations during an oral glucose tolerance test (OGTT) were determined before and six months after either intervention. Area under the curve for glucose (AUCglu) and insulin (AUCins) were calculated. DeltaIns30'/DeltaGlu30' was applied as an index of insulin secretion. The HOmeostasis Model of Assessment (HOMA) and Matsuda ISI (Insulin Sensitivity Index) were used to calculate insulin resistance (IR) and whole body insulin sensitivity, respectively. In Group 1 no difference was found in any OGTT-derived parameter. In Group 2 significant reductions in AUCins and DeltaIns30'/DeltaGlu30' were observed. No correlation between the change in DeltaCCa or DeltaPTH and DeltaAUCglu or DeltaAUCins was found in either group. Our data suggest that while subtle transient alterations of Ca and PTH within the normal range as in exogenous rhPTH 1-34 administration do not affect glucose homeostasis, the continuously elevated Ca and endogenous PTH levels as in pHPT affect insulin sensitivity and result in increased insulin secretion.