Oswald N, Binswanger U
Res Exp Med (Berl). 1979 Apr 23;175(1):19-30. doi: 10.1007/BF01851230.
Duodenal and ileal in vitro calcium transport was studied in 5/6 nephrectomized rats. Low calcium diet resulted in an increase of the duodenal calcium transport in kidney intact control animals but not in uremic rats; the ileal transport however increased in controls as well as in uremic rats. Parathyroidectomy decreased this adaptive transport at both gut sites in intact and uremic rats. Supplementation with low doses of 1,25-dihydroxycholecalciferol (1,25-DHCC) restored the duodenal transport in nephrectomized rats to the level of controls; nephrectomized plus parathyroidectomized animals increased the duodenal but not the ileal calcium transport. A close correlation between calcium transport and serum phosphorus concentrations of all groups of rats studied points towards a possible role of phosphate for intestinal calcium transport. It is concluded that duodenal calcium transport is regulated by the parathyroid-1,25-DHCC axis with 1,25-DHCC as effector; ileal calcium transport in contrast is regulated by combined direct effects of 1,25-DHCC and parathyroid hormone, the latter being essential for active transport.
对5/6肾切除大鼠的十二指肠和回肠体外钙转运进行了研究。低钙饮食导致肾脏完整的对照动物十二指肠钙转运增加,但尿毒症大鼠未增加;然而,对照大鼠和尿毒症大鼠的回肠转运均增加。甲状旁腺切除降低了完整大鼠和尿毒症大鼠两个肠道部位的这种适应性转运。补充低剂量的1,25 - 二羟胆钙化醇(1,25 - DHCC)可使肾切除大鼠的十二指肠转运恢复到对照水平;肾切除加甲状旁腺切除的动物十二指肠钙转运增加,但回肠未增加。所研究的所有大鼠组的钙转运与血清磷浓度之间密切相关,这表明磷酸盐可能在肠道钙转运中发挥作用。结论是,十二指肠钙转运由甲状旁腺 - 1,25 - DHCC轴调节,以1,25 - DHCC为效应器;相比之下,回肠钙转运由1,25 - DHCC和甲状旁腺激素的联合直接作用调节,后者对主动转运至关重要。