Abstract
The active metabolite of D vitamin, 1,25(OH) 2D 3, has been suggested to promote acute uptake of calcium through the intestinal lining in cell lines and murine models. In this study, the effects of D vitamin on the cytoplasmic Ca 2+ of single human jejunal enterocytes, obtained with LOC-I-GUT technique, was analyzed in vivo in a fluorometric system using fura-2 as the Ca 2+-sensing probe. Vitamin-promoted acute Ca 2+ influx exhibited dual kinetics, indicating initial release from intracellular Ca 2+ pools and fast entry from the extracellular space. Furthermore, providing a chemical clamp of membrane potential close to 0 mV did not activate voltage-sensitive calcium channels in the cellular membrane, neither was the hormone-induced Ca 2+ influx affected by verapamil. This advocates that voltage-operated channels like L-type Ca 2+ channels do not participate in the process of Ca 2+ uptake. In fact, the existence of calcium-release-activated-calcium channels ( I CRAC) was implied by the findings that irreversible depletion of intracellular Ca 2+ stores by thapsigargin promoted Ca 2+ entry. In the thapsigargin-treated enterocytes, D vitamin lost its ability to promote calcium entry indicating an important role for intracellular store-operated Ca 2+ stores in the acute effects of 1,25(OH) 2D 3.
Published Version
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