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  • 1
    ISSN: 1432-0827
    Schlagwort(e): 1α-Hydroxyvitamin D3 ; Vitamin D3 ; 1,25-Dihydroxyvitamin D3 receptors
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary This study was undertaken to determine whether 1α-hydroxyvitamin D3 [1α(OH)D3] administration to chicks in vivo results in 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] intestinal receptor occupancy and to compare the temporal characteristics of the physiological effects of 1α(OH)D3 and 1,25(OH)2D3 for several days after a single dose of either steroid. Occupied 1,25(OH)2D3 receptors of the chick duodenal mucosa were measured by the recently developed exchange assay procedure [J Biol Chem (1980) 255:9534–9537]. Within 2 h after 1α(OH)D3 injection in rachitic chicks, there was a significant elevation of 1,25(OH)2D3 receptor occupancy in the intestinal mucosa. This observation represents the first direct confirmation that this synthetic analog exerts biological effects through occupancy of 1,25(OH)2D3 receptors. Serum 1,25(OH)2D3 levels reached a 3-fold higher peak after 1,25(OH)2D3 injection (3.25 nmol) than after 1α(OH)D3 injection (6.5 nmol); further, after 1α(OH)D3 injection the peak was delayed by 2–4 h. However, serum 1,25(OH)2D3 levels remained elevated for only 3–6 h after 1,25(OH)2D3, compared to 48 h after 1α(OH)D3 injection. Occupied 1,25(OH)2D3 receptor levels paralleled serum 1,25(OH)2D3 levels at all times after administration of either steroid. At 24 h, duodenal vitamin D-dependent calcium binding protein (CaBP) levels were similarly elevated in both treatment groups, but by 48 and 72 h after 1α(OH)D3 administration CaBP and serum Ca2+, respectively, were more significantly elevated. These data confirm that 1α(OH)D3 induces its major biological effects via intracellular 1,25(OH)2D3 receptors and reinforce the concept that 25-hydroxylation is a prerequisite for these effects. These results also suggest that 1α(OH)D3 may become useful in the therapy for sustained treatment of vitamin D deficiency diseases.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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