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   <subfield code="a">Bone metabolic disorders caused by small bowel resection, and the influence of 1 α -hydroxyvitamin D3 on the rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Hiroshi Uno, Yoshihiro Izawa, Tamotsu Koyama, Tomohiro Ohta, Tokutaro Makita, Mitsugi Sugiyama, Norimoto Urakawa]</subfield>
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   <subfield code="a">Metabolic bone disorders caused by resection of the distal three quarters of the small bowel and the effects of 1α-hydroxyvitamin D3 (1α(OH)D3) on the rats were investigated biochemically and histomorphologically. 1α(OH)D3 was administered orally to the rats for 13 weeks. A group of &quot; sham operation” animals and the 75%-distal-small-bowel-resected control animals received only the vehicle. Bone changes developed 13 weeks after the partial bowel resection. The disorder was characterized by reductions in ash content of the femur and by the disappearance of the trabecular bone in tibial metaphysis. Decreased Ca absorption from the intestines was demonstrated by a radiotracer technique, and biochemical studies showed significant decreases in serum Ca and 1,25(OH)2D concentrations in the bowel-resected rats. These findings suggest that 75% distal small bowel resection impairs intestinal absorption of calcium and results in a negative calcium balance, which may contribute to the development of bone metabolic disorder in rats. This disorder was demonstrated as high bone turnover via urinalysis and by a radiotracer technique. Administration of 1α(OH)D3 increased dose-dependent Ca absorption from the intestine and the serum Ca, normalized the bone turnover rate and prevented the development of bone metabolic disorder.</subfield>
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