Enteroglucagon is a collective term for a small family of peptides derived from proglucagon by post-translational processing in the L-cells of the distal small intestine and colon. There is evidence that it inhibits gastric secretion, and high levels of enteroglucagon occur in plasma during intestinal adaptation, which suggests that it may also function as a trophic factor for the intestine. Certain types of soluble non-starch polysaccharide (dietary fiber) stimulate the release of enteroglucagon in rats but the mechanism is unknown. In this study we explored the importance of the viscosity and fermentability of nonabsorbed carbohydrates as determinants of plasma enteroglucagon and mucosal cell proliferation in the distal ileum of rats. Replacement of cellulose (10 g/kg) with guar gum in a semisynthetic diet led to a prompt and sustained rise in plasma enteroglucagon concentrations. Our initial hypothesis that this was a consequence of delayed nutrient absorption was disproven by the fact that hydroxypropylmethylcellulose (HPMC), a viscous but nonfermentable polysaccharide, had no effect on plasma enteroglucagon under the same conditions. In contrast, the nondigestible disaccharide lactitol led to a prolonged rise in plasma enteroglucagon, similar to that observed with guar gum. Lactitol is nonviscous, but highly fermentable, and we conclude that fermentable carbohydrate is an important stimulus for the release of enteroglucagon under our experimental conditions. There was no evidence that enteroglucagon released by this mechanism exerted trophic effects on the distal small intestinal mucosa.