Korkor A B, Kuchibotla J, Arrieh M, Gray R W, Gleason W A
Endocrinology. 1985 Dec;117(6):2267-73. doi: 10.1210/endo-117-6-2267.
Glucocorticoid inhibits intestinal calcium absorption. To further explore the mechanism of this inhibition, we studied dogs during the administration of oral prednisone (1.2-1.5 mg/kg X day) for 20 to 28 weeks in comparison to untreated dogs. Prednisone administration had no effect on serum 25-hydroxyvitamin D concentrations, but was accompanied by a fall in serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations from 87 +/- 20 pM (control) to 62 +/- 28 pM (prednisone-treated; P less than 0.01). Cytosol prepared from the duodenal, jejunal, and ileal mucosa of control dogs was found to contain a specific 3.2S [3H]1,25-(OH)2D3 binder analogous to the binder that has been observed in the intestine of other species and in other tissues. The apparent concentration of this binder decreased progressively from duodenum to ileum. Prednisone administration increased the apparent duodenal concentration of the binder from 170 +/- 91 (control) to 363 +/- 124 fmol/mg protein (prednisone-treated; P less than 0.025). The intestinal content of calcium-binding protein also declined progressively from the duodenum to the ileum, but was not affected by prednisone administration. These data suggest that events other than alterations in intestinal 1,25-(OH)2D3 receptors must mediate the inhibition of intestinal calcium absorption during chronic glucocorticoid administration.
糖皮质激素会抑制肠道对钙的吸收。为了进一步探究这种抑制作用的机制，我们对犬类进行了研究，给它们口服泼尼松（1.2 - 1.5毫克/千克×天），持续20至28周，并与未治疗的犬类作比较。给予泼尼松对血清25 - 羟基维生素D浓度没有影响，但伴随着血清1,25 - 二羟基维生素D [1,25 - (OH)₂D]浓度从87±20皮摩尔（对照）降至62±28皮摩尔（泼尼松治疗组；P＜0.01）。从对照犬的十二指肠、空肠和回肠黏膜制备的胞质溶胶中，发现含有一种特异性的3.2S [³H]1,25 - (OH)₂D₃结合蛋白，类似于在其他物种的肠道和其他组织中观察到的结合蛋白。这种结合蛋白的表观浓度从十二指肠到回肠逐渐降低。给予泼尼松使十二指肠中这种结合蛋白的表观浓度从170±91（对照）增加到363±124飞摩尔/毫克蛋白（泼尼松治疗组；P＜0.025）。钙结合蛋白的肠道含量也从十二指肠到回肠逐渐下降，但不受泼尼松给药的影响。这些数据表明，在长期给予糖皮质激素期间，除了肠道1,25 - (OH)₂D₃受体改变之外的其他事件必定介导了对肠道钙吸收的抑制作用。
