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pubmed-article:2721448pubmed:abstractTextUptake of Ca2+ in cells isolated from rat duodenum declined in the senescent rats. This age-related change was not due to an alteration in the rate of Ca2+ efflux or in the size of the cell. The decrease appeared specific, as alpha-methyl glucoside uptake was not altered. Cell population, as monitored by sucrase activity for villus cells, was not different between duodenal cells isolated from 6- and 24-month-old rats. Kinetic analysis shows the Vmax, the apparent maximum uptake capacity, decreased in the cells from senescent rats whereas the Km, the apparent affinity to Ca2+, was unchanged. Serum levels of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] were determined as a function of age; the levels of 25OHD were not significantly different in 3-, 6-, 12-, and 24-month-old rats. On the other hand, serum 1,25-(OH)2D decreased throughout the age range studied. Since duodenal Ca2+ uptake is closely regulated by 1,25-(OH)2D3, we tested the hypothesis that low serum 1,25-(OH)2D in the senescent rats may have contributed to the decline in duodenal Ca2+ uptake. In vivo administration of 1,25-(OH)2D3 to senescent rats significantly enhanced Ca2+ uptake activity in the isolated duodenal cells. After 1,25-(OH)2D3 treatment, Ca2+ uptake activity in cells isolated from senescent rats was only slightly less than that in cells from adult rats. We conclude that duodenal Ca2+ uptake declined in the senescent rats, and this age-related change was most likely due to the low serum level of 1,25-(OH)2D and not the result of a decrease in any duodenal response to 1,25-(OH)2D3.lld:pubmed
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pubmed-article:2721448pubmed:volume124lld:pubmed
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pubmed-article:2721448pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:2721448pubmed:year1989lld:pubmed
pubmed-article:2721448pubmed:articleTitleEffect of age on calcium uptake in isolated duodenum cells: role of 1,25-dihydroxyvitamin D3.lld:pubmed
pubmed-article:2721448pubmed:affiliationLaboratory of Biological Chemistry, Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224.lld:pubmed
pubmed-article:2721448pubmed:publicationTypeJournal Articlelld:pubmed
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