What is the essential role in the normalized rat intestinal transit? Calcium or calcitonin

Both calcium and calcitonin have been involved in mediating gastrointestinal motility. Using a thyroidectomized rat model the present study tried to determine which one of them was essential for normal small intestinal transit.

Adult Sprague-Dawley male rats simultaneously received thyroidectomy or a sham operation plus a laparotomy for duodenal tubing. After two-week housing, a small intestinal transit study was conducted via geometric center computation of radioactivities of the intestinal segments counted from intraduodenal feeding of radiochromium. Before feeding, these rats were i.p. injected with saline or human calcitonin in the doses of 0.1, 1 and 10 microM/kg, respectively. Another group of Tx rats received i.v. infusion of saline or CaCl2 for 30 min before motility study.

Thyroidectomization effectively delayed transit compared to the sham-operated controls (3.59 +/- 0.15 vs. 2.98 +/- 0.32, P < 0.05). High doses of calcitonin treatment in thyroidectomized rats further inhibited transit (P < 0.01), whereas calcitonin did not restore the suppressed calcium level. Delayed transit in thyroidectomized rats was restored after calcium infusion (2.95 +/- 0.22 vs. 3.78 +/- 0.42, P < 0.05) while their hypocalcemia was already corrected.

Thyroidectomization disturbs small intestinal transit, while peripheral calcitonin replacement further inhibits transit. Since calcium replacement enables to restore small intestinal transit, it is apparent that calcium rather than calcitonin is essential for normal small intestinal transit.