Postprandial stimulation of epithelial cell proliferation in defunctioned colon of rats is not caused by gastrin

Abstract

Rats were submitted, at random, to either a diverting colostomy alone or to antrectomy with a colostomy. After a 48-h fasting period, animals from each group were refed, whereas control animals were kept fasting. Animals were killed at 0, 6, 12, 18, and 24 h after the time of refeeding. In vitro labeling of colon mucosa with [3H]thymidine and autoradiography were performed to determine the proliferative parameters in the colonic crypts, and scintillation counts on mucosal scrapings were used for the estimation of mucosal deoxyribonucleic acid synthetic activity. Refeeding increased the labeling index (p less than 0.01), mitotic index (p less than 0.01), and mucosal deoxyribonucleic acid synthesis activity (p less than 0.01) in the proximal colon as well as in the defunctioned distal segment. Despite suppression of the postprandial rise in serum gastrin (p less than 0.01), antrectomy did not abolish the proliferative reaction in any colonic segment. These data confirm the existence of a potent stimulant of colonic cell proliferation that is released systematically after feeding. They indicate that gastrin is not the responsible stimulant and that another, yet unknown, physiological factor is involved.