Interaction between Calcium, Calciotropic Hormones and the Gastrin-ECL-cell Axis

Abstract: Calcium homeostasis involves mainly the interaction of PTH, vitamin D and CT. The stomach may be important for calcium homeostasis. Gastric acid is thought to mobilize calcium from the diet, thereby facilitating the absorption of calcium in the small intestines. In the rat, gastrectomy rapidly reduces the calcium content, the density and the trabecular volume of the bone. The gastrectomy-evoked bone loss cannot be prevented by supplementation with CaCl2 and it is unlikely to reflect either calcium or vitamin D deficiency. It may reflect the lack of a calciotropic or osteotropic hormone, that emanates from the oxyntic mucosa. Gastrin has been suggested to release a hypocalcemic peptide hormone, gastrocalcin, from the oxyntic mucosal ECL cells, which is thought to act to enhance the uptake of Ca into bone. Gastrin has also been suggested to have a growth-promoting effect on the parathyroid gland. The present study examines the possibility that the gastrin-ECL-cell axis is integrated with known regulatory systems for calcium and bone metabolism. Omeprazole treatment, which activates the gastrin-ECL-cell axis, was associated with hypertrophy and hyperplasia of the chicken parathyroid glands. Dietary calcium seems to enhance the release of gastrin without activating the ECL cells of the rat stomach. Acute perturbations in circulating calcium did not affect either the release of gastrin or the activity of the ECL cells in the rat. Short-term administration of PTH or CT had no effect on the serum gastrin concentration or on the activity of the ECL cells. Vitamin D suppressed the activity of the ECL cells, presumably via vitamin D receptors in the oxyntic mucosa.The gastrin-ECL-cell axis appears to be functionally integrated with vitamin D-dependent and PTH-dependent regulatory systems and may play a role in bone metabolism.