Glicentin, an active enteroglucagon, has a significant trophic role on thesmall intestine but not on the colon in the rat

Background: Many experiments have indicated that the gut glucagons (enterog lucagons) are associated with cell proliferation in the small intestine. Ho wever, recent studies have failed to show trophic effects of glicentin (ent eroglucagon) on the intestine. Aims: To examine the effects of glicentin on intestinal proliferation in vi vo in the rat. Methods: Rats were established on total parenteral nutrition for 6 days. Fo ur experimental groups were given daily doses of 1, 4, 20 and 80 mug/rat of glicentin via the jugular vein. Rats fed by total parenteral. nutrition an d rats fed chow ad libitum were used as controls. Tissues taken from the du odenum, jejunum, ileum and colon were fixed in Carnoy's fluid and microdiss ected to determine the metaphase arrest scores and crypt fission ratios. Results: The mean metaphase arrest scores per crypt of the small intestine were significantly increased in the rats given 4, 20 and 80 mug of glicenti n. These responses were dose-dependent, and were most prominent in the ileu m. Crypt fission of the ileum was significantly decreased in the 20 and 80 mug glicentin groups. Glicentin had no effects on proliferation or fission in the colon. Conclusions: Glicentin is trophic to the rat small intestine, but not the c olon.