The effects of Secretin (3.5 U/100 g) and Pentagastrin (25 μg/l00 g) on cell renewal in jejunal mucosa was studied in male Wistar rats. The labeling index (LI), mitotic index (MI), and histogram of the distribution of labeled cells were measured at 4-hour intervals during 24 h after intraperitoneal injection of hormones and compared with results obtained in control animals. DNA label was obtained by injection of tritiated thymidine (70 μCi/100 g) 30 min before sacrificing the animals. The proliferation of intestinal cells in rats was marked by a circadian rhythm with a nocturnal peak of DNA synthesis. After Pentagastrin, the LI remained high for 16,20, and 24 h after injection, during the time the control levels diminished in the circadian rhythm. The normal MI and the enlargement of the zone of proliferation support the hypothesis of a stimulating effect of gastrin on intestinal cell renewal. After Secretin, the LI peak of the cycle was suppressed and the MI decreased, indicating an inhibiting effect of Secretin on intestinal cell renewal. Secretin and gastrin act as trophic factors on intestinal mucosa and produce opposite effects on cell proliferation.

No abstract

In the cat, gastric lipase secretion was equally but weakly stimulated by pentagastrin, a major stimulant of acid secretion, and by carbamylcholine, a major stimulant of pepsin secretion. Lipase was also stimulated by fresh liver, which induces a large blood gastrin release and not by canned food, which is a poor gastrin releaser. Lipase output always preceded that of acid an pepsin. Lipase was not correlated with acid and pepsin secretion while acid and pepsin were well correlated during all stimulations but not in basal state. Lipase is co-localized with pepsin in the chief cells but is also present in pepsin-free cells, the mucus surface cells of the fundus and the antrum. The distribution of lipase explains the lack of correlation between pepsin and lipase as already mentioned. However, our data show that lipase secretion is under the control of gastric stimulants and might play a role in the gastric initiation of pancreatic meal lipolysis.