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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #214685
Title: Activation of the calcium sensing receptor stimulates serum gastrin and gastric acid secretion in healthy subjects

Author
item CEGLIA, LISA - TUFTS UNIVERSITY HNRCA
item HARRIS, SUSAN - TUFTS UNIVERSITY HNRCA
item RASMUSSEN, HELEN - TUFTS UNIVERSITY HNRCA
item Dawson-Hughes, Bess

Submitted to: Osteoporosis International
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/11/2008
Publication Date: 6/2/2008
Citation: Ceglia, L., Harris, S., Rasmussen, H.M., Dawson-Hughes, B. 2008. Activation of the calcium sensing receptor stimulates serum gastrin and gastric acid secretion in healthy subjects . Osteoporosis International. DOI 10.1007/s00198-008-0637-8.

Interpretive Summary: Acid production by the stomach helps to digest food and it also promotes the absorption of calcium. It has long been known that calcium supplements increase stomach acid but the mechanism for this process is unknown. In this 18-day study in 17 healthy men and women, we assessed the effect of activation of the calcium sensing receptor on gastric acid production. When compared with placebo, the receptor activator, cinacalcet, significantly increased stomach acid production. This study provides an explanation for how increasing calcium intake promotes gastric acid production in humans.

Technical Abstract: Gastric acid secretion is a complex process regulated by neuronal and hormonal pathways. Ex vivo studies in human gastric tissues indicate that the calcium sensing receptor (CaR), expressed on the surface of G and parietal cells, may be involved in this regulation. We sought to determine whether cinacalcet, a CaR allosteric agonist, increases serum gastrin levels and gastric acid secretion. The study we conducted was an 18-day randomized placebo-controlled double-blind trial with a fixed metabolic diet in a metabolic research unit at an academic medical center. Seventeen healthy subjects age 45-70 with normal gastric acid output participated in the study. Exclusion criteria included diseases and medications known to affect gastric acid and calcium balance. On day 8 (baseline), subjects were given cinacalcet (15 then 30 mg daily) or placebo for 11 days. Basal and maximal gastric acid output and serum gastrin level were the main outcome measures. Study results showed that baseline basal and maximal gastric acid output and serum gastrin levels were similar between groups. However, changes in serum gastrin and basal acid output (adjusted for baseline weight) were significantly more positive in the cinacalcet group compared to placebo (P=0.004 and P=0.039, respectively). Change in maximal acid output was similar in the 2 groups (P=0.995). As expected, cinacalcet produced significant decreases in serum PTH (P<0.001) and ionized calcium levels (P=0.032), and increases in serum phosphorus levels (P=0.001) and urinary calcium excretion (P=0.023). This study provides in vivo evidence that activation of the CaR increases serum gastrin levels and basal gastric acid secretion in healthy adults.