Journal
NUTRITION REVIEWS
Volume 69, Issue 7, Pages 347-370Publisher
OXFORD UNIV PRESS INC
DOI: 10.1111/j.1753-4887.2011.00395.x
Keywords
calcium transport; gastrointestinal tract; glucose transport; nutrition
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Funding
- Wellcome Trust [062541/Z/00, 064302/Z/01]
- Biotechnology and Biological Sciences Research Council, UK [BB/C51300X/1]
- Biotechnology and Biological Sciences Research Council [BB/C51300X/1] Funding Source: researchfish
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Transcellular models of dietary Ca2+ absorption by the intestine assign essential roles to TRPV6 and calbindin-D-9K. However, studies with gene-knockout mice challenge this view. Something fundamental is missing. The L-type channel Ca(v)1.3 is located in the apical membrane from the duodenum to the ileum. In perfused rat jejunum in vivo and in Caco-2 cells, Ca(v)1.3 mediates sodium glucose transporter 1 (SGLT1)-dependent and prolactin-induced active, transcellular Ca2+ absorption, respectively. TRPV6 is activated by hyperpolarization and is vitamin D dependent; in contrast, Ca(v)1.3 is activated by depolarization and is independent of calbindin-D9K and vitamin D. This review considers evidence supporting the idea that Ca(v)1.3 and TRPV6 have complementary roles in the regulation of intestinal Ca2+ absorption as depolarization and repolarization of the apical membrane occur during and between digestive periods, respectively, and as chyme moves from one intestinal segment to another and food transit times increase. Reassessment of current arguments for paracellular flow reveals that key phenomena have alternative explanations within the integrated Ca(v)1.3/TRPV6 view of transcellular Ca2+ absorption. (C) 2011 International Life Sciences Institute
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