Effects of 1,25‐dihydroxycholecalciferol administration on the rat renal vitamin K‐dependent carboxylating system

FEBS Letters

Karl, Peter I.¹  Friedman, Paul A.¹  Carnes, David L.² 

[1] Department of Pharmacology, Harvard Medical School, Charles A. Dana Research Institute, Harvard-Thorndike Laboratory of Beth Israel Hospital, Department of Medicine, Beth Israel Hospital, Harvard Medical School, Israel;The Children's Hospital Medical Center, Department of Medicine, Endocrine Division, Boston, MA 02215, USA

关键词: γ-Glutarnyl carboxylase;    Substrate;    Vitamin K;    Kidney;    1;    25-Dihydroxycholecalciferol;    Gla;    γ-carboxyglutamic acid;    BGP;    bone Gla protein;    1;    25(OH)2D3;    1;    25-dihydroxycholecalciferol;    PTH;    parathyroid hormone;    FLEEL;    the pentapeptide phenylalanyl-leucyl-glutamyl-glutamyl-leucine;   

DOI  :  10.1016/0014-5793(85)80116-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We have shown previously that the in vitro activity of the renal vitamin K-dependent γ-glutamyi carboxylase toward synthetic oligopeptide substrates is stimulated by administration of either parathyroid hormone (PTH) or 1,25-dihydroxycholecalciferol [1,25 (OH)₂D₃] to rats [(1983) J. Biol. Chem. 258, 12783-12786]. Here we report that administration of 1,25(OH)₂D₃ to rats increases their levels of endogenous carboxylase substrate as well. Rats fed a vitamin D-deficient diet had highly elevated serum PTH levels while vitamin D-replete animals had undetectable levels. Furthermore, since PTH increases 1,25(OH)₂D₃ levels by stimulating renal 25-hydroxy vitamin D-1α-hydroxylase, it is very likely that the stimulatory effects of PTH on the renal vitamin K-dependent carboxylating system are mediated by 1,25(OH);,D3.

【 授权许可】

Unknown