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Clinical Trial Summary

We have established that dietary protein is an important regulator of intestinal calcium absorption in humans. However, we do not understand the mechanism by which dietary protein is affecting calcium absorption. Therefore, the purpose of this research is to evaluate whether dietary protein-induced changes in gastric acid secretion explain the observed changes in intestinal calcium absorption.


Clinical Trial Description

We have established that dietary protein is an important regulator of intestinal calcium absorption in humans. However, we do not understand the mechanism by which dietary protein is affecting calcium absorption. Therefore, the purpose of this research is to evaluate whether dietary protein-induced changes in gastric acid secretion explain the observed changes in intestinal calcium absorption. We have compelling in vitro data that amino acids can stimulate gastric acid secretion. We have found that this occurs via allosteric activation of the calcium sensing receptor expressed on the gastric acid-secreting parietal cells. At a fixed concentration of extracellular calcium, addition of L but not D isomers of specific amino acids activates the calcium sensing receptor and stimulates parietal cell acid production. We hypothesize that dietary protein induced gastric acid production increases calcium solubility and bioavailability thereby increasing its absorption. We will test this hypothesis in humans by quantifying the impact of dietary protein on intestinal calcium absorption in subjects who cannot make gastric acid. We will measure intestinal calcium absorption in healthy adults as they consume either a high protein diet with concomitant administration of a proton pump inhibiting (PPI) drug or the same high protein diet with a placebo instead of a PPI. The order of the 2 interventions will be randomized, and study will be double-blind and placebo controlled. If our hypothesis is correct, then intestinal calcium absorption will be highest during the high protein diet with placebo, and lowest during the drug intervention. ;


Study Design


Related Conditions & MeSH terms


NCT number NCT00719160
Study type Interventional
Source Yale University
Contact
Status Completed
Phase Phase 4
Start date January 2005
Completion date May 2008

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