The parathyroid polyhormone hypothesis revisited.
The parathyroid polyhormone hypothesis holds that peptides derived from the metabolism of parathyroid hormone ( PTH) (so-called C-terminal fragments) are themselves biologically active and that their effects are mediated by a novel 'C-terminal receptor.' The evidence supporting these assertions is extensive but remains inconclusive. This Commentary focuses on in vivo pharmacology studies that provide information relevant to understanding the physiological significance of C-terminal fragments. The more recent studies of this sort provide compelling evidence that the bioactivity of C-terminal fragments is likely to become physiologically relevant in settings of secondary hyperparathyroidism. In this condition, circulating levels of C-terminal fragments greatly exceed those of PTH. There is convincing evidence that the hypocalcemic effect of C-terminal fragments results from direct actions on the skeleton that inhibit bone resorption. On the other hand, there are few if any results of in vivo studies suggesting a role for C-terminal fragments in more physiological settings, at least when parameters associated with systemic calcium homeostasis are assessed.[1]References
- The parathyroid polyhormone hypothesis revisited. Nemeth, E.F. Kidney Int. Suppl. (2006) [Pubmed]
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