Pattern of cell proliferation and enteroglucagon response following small bowel resection in the rat.
Gut resection triggers off a complex series of adaptive changes in the remaining bowel. There is evidence that these are partly mediated by hormonal factors and enteroglucagons have been proposed as candidates for this role. It is uncertain, however, whether plasma enteroglucagon concentrations rise quickly enough to be involved in the rapid initial response or are persistent enough for chronic maintenance. Plasma concentrations of enteroglucagon were therefore estimated at varying times following gut resection and related to crypt cell production rate (CCPR), which was used as an index of cellular proliferation. 96 male Wistar rats had either 75% proximal small bowel resection or jejunal transection (controls). Groups of animals were killed at 1.5, 3, 6, 12, 24 and 48 days following operation and the plasma enteroglucagon and CCPR in the terminal ileum were estimated. Both values were markedly elevated at 1.5 days and continued to rise in a very similar manner in the resected group of rats. Gel permeation chromatography on Sephadex G-50 of plasma samples showed that the increase in plasma enteroglucagon was mainly due to an increase in a component of Kav 0.25, of similar molecular size to that of porcine glicentin. Thus the principal form of enteroglucagon, as a possible trophic hormone, does respond sufficiently quickly, and the response is maintained for long enough, to be involved throughout the adaptive process.