Chan S D, Chiu D K, Atkins D
J Endocrinol. 1984 Dec;103(3):295-300. doi: 10.1677/joe.0.1030295.
The distribution of 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) receptors in isolated jejunal villous and crypt cells was investigated in normal and adrenalectomized male rats, and also in animals treated with the synthetic glucocorticoid, dexamethasone, and/or the glucocorticoid antagonist, 11-deoxy-cortisol. Adrenalectomy caused an increase in 1,25-(OH)2D3 receptors whilst dexamethasone treatment led to a reduction in receptor number. 11-Deoxy-cortisol was able to reverse the 'down-regulation' effect caused by glucocorticoids. In all cases, the changes in receptor numbers were more pronounced in crypt cells. The data suggest that, in the small intestine, glucocorticoids may control the synthesis of 1,25-(OH)2D3 receptors via the mediation of a glucocorticoid receptor, and that the adrenal hormones mainly express their effect in crypt cells. It is proposed that this phenomenon may, in part, explain the reduction in calcium absorption which occurs in man after chronic glucocorticoid treatment.
研究了正常和肾上腺切除的雄性大鼠，以及用合成糖皮质激素地塞米松和/或糖皮质激素拮抗剂11-脱氧皮质醇处理的动物中，1α,25-二羟基维生素D3（1,25-(OH)2D3）受体在分离的空肠绒毛和隐窝细胞中的分布。肾上腺切除术导致1,25-(OH)2D3受体增加，而地塞米松治疗导致受体数量减少。11-脱氧皮质醇能够逆转糖皮质激素引起的“下调”效应。在所有情况下，隐窝细胞中受体数量的变化更为明显。数据表明，在小肠中，糖皮质激素可能通过糖皮质激素受体的介导来控制1,25-(OH)2D3受体的合成，并且肾上腺激素主要在隐窝细胞中发挥作用。有人提出，这种现象可能部分解释了慢性糖皮质激素治疗后人类钙吸收减少的原因。
