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- W2068490149 abstract "1. Experiments were carried out to elucidate some of the biochemical consequences of vitamin D administration, in vivo, in its target organ, the intestinal mucosa. Oral administration of 500 I.U. of vitamin D3 (cholecalciferol) to vitamin D-deficient chicks causes the level of alkaline phosphatase (orthophosphoric monoester phosphohydrolase, EC 3.1.3.1) of intestinal mucosal homogenates to increase 2–3-fold. The increased level of intestinal alkaline phosphatase activity is maximal 60 h after the administration of the vitamin. 2. The intestinal alkaline phosphatase(s) of both vitamin D-deficient and vitamin D-treated chicks is localized exclusively in the brush border or microvilli fraction, the site of many intestinal absorption activities. Also the brush border levels of Ca2+-stimulated ATPase (ATP phosphohydrolase, EC 3.6.1.3) are elevated after vitamin D administration; however, vitamin D treatment causes no change in the levels of investase (δ-d-fructofuranoside fructohydrolase, EC 3.2.1.26) and other related disaccharidases which are localized in the intestinal brush border fraction. 3. The rise in intestinal brush border alkaline phosphatase mediated by vitamin D can be prevented by the administration in vivo of cycloheximide. This suggests that the vitamin induces the de novo synthesis of this enzyme. 4. The simultaneous time-course of appearance of (a) increased levels of brush border alkaline phosphatase and (b) the increased rate of transport of calcium, measured in vivo across intact segments of ileal tissue after oral vitamin D3 administration, suggests a functional involvement of alkaline phosphatase in vitamin D-mediated calcium transport." @default.
- W2068490149 created "2016-06-24" @default.
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- W2068490149 date "1970-08-01" @default.
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- W2068490149 title "Studies on the mechanism of action of calciferol III. Vitamin D-mediated increase of intestinal brush border alkaline phosphatase activity" @default.
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- W2068490149 doi "https://doi.org/10.1016/0304-4165(70)90034-6" @default.
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