Ospedale Casa Sollievo della Sofferenza, IRCCS, San Giovanni Rotondo, Foggia, Italy.
J Endocrinol Invest. 2011 Jul;34(7 Suppl):23-6.
Carboxyl-terminal PTH fragments (C-PTH), are generated by both direct secretion from parathyroids in relation to serum calcium levels and catabolism of PTH operated by the Kupffer cells in the liver. These molecular fragments have been till recently regarded as inert byproducts of PTH metabolism, since they do not interact with the PTH/PTH-related peptide (rP) receptor, which mediates the classical hormone actions. Current findings instead indicate that C-PTH would interact with a putative C-PTH receptor. This way, C-PTH seem to exert specific effects on calcium homeostasis and bone metabolism, opposite to those of the synthetic agonist of PTH/PTHrP receptor (i.e. PTH 1-34). In vitro and in vivo data actually indicate that C-PTH, by interacting with specific receptors, could have an anti-calcemic action, as well as a pro-apoptotic effect on both osteocytes and osteoclasts. This in turn could result in a reduced activity of the latter cells, with a consequent inhibition of bone resorption.
羧基末端甲状旁腺素片段(C-PTH)是由甲状旁腺根据血清钙水平直接分泌以及肝脏中的枯否细胞进行代谢分解而产生的。直到最近,这些分子片段还被认为是 PTH 代谢的无活性副产物,因为它们不与 PTH/PTH 相关肽 (rP) 受体相互作用,而后者介导了经典的激素作用。目前的研究结果表明,C-PTH 可能与假定的 C-PTH 受体相互作用。这样,C-PTH 似乎对钙稳态和骨代谢产生特定的影响,与 PTH/PTHrP 受体的合成激动剂(即 PTH1-34)的作用相反。实际上,体外和体内数据表明,C-PTH 通过与特定受体相互作用,可能具有抗钙作用,以及对成骨细胞和破骨细胞的促凋亡作用。这反过来又可能导致后者细胞活性降低,从而抑制骨吸收。