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Metabolism of 25-hydroxyvitamin D in copper-laden rat: A model of Wilson's disease

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:6948881
; ;  [1]
  1. Harvard Medical School, Boston (USA) Yale Univ. School of Medicine, New Haven, CT (USA)
Wilson's disease results in excess tissue accumulation of copper and is often complicated by skeletal and mineral abnormalities. The authors investigated vitamin D metabolism in rats fed a copper-laden diet rendering hepatic copper content comparable with that found in Wilson's disease. Injection of 25-hydroxyvitamin D{sub 3} (25(OH)D{sub 3}) resulted in reduced 1,25--dihydroxyvitamin D (1,25(OH){sub 2}D) levels in copper-intoxicated rats. In vitro 25(OH)D-1{alpha}-hydroxylase activity was impaired in renal mitochondria from copper-intoxicated animals. Activity was also inhibited in mitochondrial from controls when copper was added to incubation media. Impaired conversion of 25(OH)D to 1,25(OH){sub 2}D occurs in copper intoxication and suggests that altered vitamin D metabolism is a potential factor in the development of bone and mineral abnormalities in Wilson's disease.
OSTI ID:
6948881
Journal Information:
American Journal of Physiology; (USA), Journal Name: American Journal of Physiology; (USA) Vol. 254:2; ISSN 0002-9513; ISSN AJPHA
Country of Publication:
United States
Language:
English