The Effect of Protein on Calcium Absorption and Gastric Acid Production
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Purpose
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.
| Condition | Intervention | Phase |
|---|---|---|
|
Osteoporosis |
Drug: esomeprazole Drug: Placebo |
Phase 4 |
| Study Type: | Interventional |
| Study Design: | Allocation: Randomized Endpoint Classification: Efficacy Study Intervention Model: Crossover Assignment Masking: Double Blind (Subject, Caregiver, Investigator) Primary Purpose: Treatment |
| Official Title: | Dietary Protein's Effect on Gastric pH and Calcium Absorption |
- Percent Change in Intestinal Calcium Absorption [ Time Frame: Day 5 of a high protein diet ] [ Designated as safety issue: No ]This is completed by measuring the amount of calcium absorbed by utilizing dual stable calcium isotopes. It was hypothesized that we would see a percent decrease as a result of the proton pump inhibitor. Previous published data indicated a decline in calcium absorption of 6.6 +/- 5.5% when gastric pH is blocked.
- Gastric pH [ Time Frame: Day 5 of a high protein diet ] [ Designated as safety issue: No ]The American Heritage Dictionary defines pH as "a measure of the acidity or alkalinity of a solution, numerically equal to 7 for neutral solutions, increasing with increasing alkalinity and decreasing with increasing acidity. The pH scale commonly in use ranges from 0 to 14." The normal pH range for stomach acid is between 1.5 and 3.5.
| Enrollment: | 12 |
| Study Start Date: | January 2005 |
| Study Completion Date: | May 2008 |
| Primary Completion Date: | May 2008 (Final data collection date for primary outcome measure) |
| Arms | Assigned Interventions |
|---|---|
| Placebo Comparator: Esomeprazole |
Drug: esomeprazole
2 Interventions with esomeprazole 20 mg twice a day for 9 days vs. a placebo for 9 days while on a high protein diet
Drug: Placebo
Placebo 20 mg twice a day for 9 days
|
| Active Comparator: Placebo |
Drug: esomeprazole
2 Interventions with esomeprazole 20 mg twice a day for 9 days vs. a placebo for 9 days while on a high protein diet
Drug: Placebo
Placebo 20 mg twice a day for 9 days
|
Detailed 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.
Eligibility| Ages Eligible for Study: | 18 Years to 45 Years |
| Genders Eligible for Study: | Both |
| Accepts Healthy Volunteers: | Yes |
Inclusion Criteria:
- Healthy men and women age 18-45 years
- Caucasian or Asian descent due to increased risk of Osteoporosis
Exclusion Criteria:
- gastrointestinal diseases
- osteoporosis
- diabetes
- hypertension
- liver disease
- thyroid disorders
- kidney disease
- kidney stones
- cancer
- heart disease
- eating disorders
- obesity
- hypogonadism
- amenorrhea
- oligomenorrhea
- abnormal serum FSH or estradiol levels
- birth control medication or other hormone-altering medications
- pregnancy
Lifestyle factors such as:
- smoking
- excessive exercise (although moderate exercise is allowed)
- prescription medications known to influence vitamin D or calcium metabolism or gastric acid
- excessive body weight change during the past 6 months
- food allergies
- unusual eating habits or medically prescribed diets
Contacts and Locations| United States, Connecticut | |
| Yale New Haven Hospital Hospital Research Unit | |
| New Haven, Connecticut, United States, 06510 | |
| Principal Investigator: | Karl Insogna, MD | Yale University |
More Information
No publications provided
| Responsible Party: | Karl Insogna, Professor of Medicine, Yale University |
| ClinicalTrials.gov Identifier: | NCT00719160 History of Changes |
| Other Study ID Numbers: | 0408026977 |
| Study First Received: | July 17, 2008 |
| Results First Received: | January 26, 2012 |
| Last Updated: | November 30, 2012 |
| Health Authority: | United States: Institutional Review Board |
Keywords provided by Yale University:
|
Gastric acid Dietary protein Calcium Intestinal absorption Calcium sensing receptor |
Additional relevant MeSH terms:
|
Osteoporosis Bone Diseases, Metabolic Bone Diseases Musculoskeletal Diseases Omeprazole Anti-Ulcer Agents |
Gastrointestinal Agents Therapeutic Uses Pharmacologic Actions Enzyme Inhibitors Molecular Mechanisms of Pharmacological Action |
ClinicalTrials.gov processed this record on June 18, 2013