Effect of glucocorticoid administration on intestinal, renal, and cerebellar calbindin-D28K in chicks

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Abstract
A radioimmunoassay for chick intestinal calcium-binding protein (calbindin-D28K, CaBP-28K) has been developed in our laboratory with a detection limit of 0.3 ng/ml. The values for CaBP-28K in vitamin D-deficient (-D) chicks ranged from a high value for the cerebellum (21,400 ± 580 ng/mg protein) to a scarcely detectable level in the liver (19.6 ± 2.2 ng/mg protein). After administration of vitamin D (vitamin D3 500 IU p.o. for 7 days) (+ D), the levels of CaBP-28K increased in the duodenum (52,300 ± 5,100 ng/mg protein), ileum (45,200 ± 740 ng/mg protein), cerebellum (22,000 ± 470 ng/mg protein), colon (15,200 ± 330 ng/mg protein), and kidney (13,460 ± 540 ng/mg protein). However, the increment in the level of CaBP-28K in each tissue after vitamin D administration was different; levels of CaBP-28K in the duodenum, ileum, and colon increased dramatically more than 200 times after vitamin D administration, whereas that in the kidney showed only a 2.5-fold increase and was unaltered in the cerebellum. On the other hand, glucocorticoid administration (dexamethasone, 1 mg/kg BW i.m. for 2 days) markedly inhibited the vitamin D-stimulated (vitamin D3 500 IU p.o. for 3 days) levels of CaBP-28K in the duodenum (from 23,373 ± 3,117 to 8,261 ± 968 ng/mg protein, p < 0.001), ileum (from 6,443 ± 1,342 to 3,712 ± 691 ng/mg protein, p < 0.01), and colon (from 4,335 ± 174 to 2,316 ± 590 ng/mg protein, p < 0.01. whereas glucocorticoid further increased the vitamin D-stimulated level of CaBP-28K in the kidney (from 3,922 ± 776 to 5,593 ± 450 ng/mg protein, p < 0.01). The level of CaBP-28K in the cerebellum was unaffected either in the presence or absence of vitamin D or glucocorticoid. Although the precise action of glucocorticoid on CaBP-28K is still unclear, these results indicate that glucocorticoid is inhibitory in the intestine and colon, but is augmentative in the kidney, promoting an increase in the vitamin D-stimulated CaBP-28K production. However, glucocorticoid did not affect the level of CaBP-28K in the cerebellum, irrespective of the presence or absence of vitamin D, suggesting a vitamin D- and glucocorticoid-independent control mechanism for CaBP-28K production in the cerebellum. As a final observation, bidirectional regulatory mechanisms of the vitamin D-dependent CaBP-28K may exist in chicks, one stimulatory, the other inhibitory.
Funding Information
  • Fundamental Scientific Research, Japan