Yeh J K, Aloia J F, Semla H M
Calcif Tissue Int. 1984 Sep;36(5):608-14. doi: 10.1007/BF02405375.
The interrelation of glucocorticoids and 1,25 dihydroxycholecalciferol (1,25(OH)2D3) on intestinal calcium and phosphate absorption was investigated. The active and passive transport of calcium and phosphate was evaluated by the in situ intestinal loop technique. Administration of cortisone resulted in a decrease of the luminal fluid and an increase of the luminal calcium and phosphate concentration. Under active transport conditions, administration of cortisone resulted in a decrease of net calcium absorption through two mechanisms: (1) depressed vitamin D-dependent calcium absorption, (2) increased vitamin D-independent calcium backflux. The enhancement of bidirectional phosphate flux by cortisone was independent of 1,25(OH)2D3. An enhancement of water movement by cortisone resulted in an increase of luminal calcium and phosphate concentration which favors the passive diffusion of these ions. Enhanced calcium diffusion by cortisone compensates for the inhibitory effect of cortisone on vitamin D-dependent calcium transport. However, enhanced phosphate diffusion by cortisone is additive to the effect of 1,25(OH)2D3.
研究了糖皮质激素与1,25-二羟胆钙化醇（1,25(OH)₂D₃）对肠道钙和磷吸收的相互关系。采用原位肠袢技术评估钙和磷的主动及被动转运。给予可的松导致肠腔液减少，肠腔钙和磷浓度升高。在主动转运条件下，给予可的松通过两种机制导致净钙吸收减少：（1）抑制维生素D依赖的钙吸收，（2）增加维生素D非依赖的钙回流。可的松对双向磷通量的增强与1,25(OH)₂D₃无关。可的松对水运动的增强导致肠腔钙和磷浓度升高，有利于这些离子的被动扩散。可的松增强的钙扩散补偿了可的松对维生素D依赖的钙转运的抑制作用。然而，可的松增强的磷扩散与1,25(OH)₂D₃的作用相加。
