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Effect of glucocorticoid administration on intestinal, renal, and cerebellar calbindin‐D 28K in chicks
Author(s) -
Tohmon Miyo,
Fukase Masaaki,
Kishihara Michizo,
Kadowaki Seizo,
Fujita Takuo
Publication year - 1988
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650030312
Subject(s) - medicine , endocrinology , ileum , vitamin , duodenum , cholecalciferol , chemistry , kidney , radioimmunoassay , calbindin , vitamin d and neurology , calcium , biology
Abstract A radioimmunoassay for chick intestinal calcium‐binding protein (calbindin‐D 28K , 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 D 3 500 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 D 3 500 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.