Effects of an elemental diet, inert bulk and different types of dietary fibre on the response of the intestinal epithelium to refeeding in the rat and relationship to plasma gastrin, enteroglucagon, and PYY concentrations.

Abstract

SUMMARY Refeeding starved rats with an elemental diet resulted in a marked increase in crypt cell production rate (CCPR) in the proximal small intestine but not in the distal regions of the gut. Little effect on CCPR was noted when inert bulk (kaolin) was added to the elemental diet. Addition of a poorly fermentable dietary fibre (purified wood cellulose) had little effect on intestinal epithelial cell proliferation except in the distal colon where it significantly increased CCPR. A more readily fermentable fibre (purified wheat bran) caused a large proliferative response in the proximal, mid, and distal colon and in the distal small intestine. A gel forming fibre only significantly stimulated proliferation in the distal colon; the rats in this group, however, did not eat all the food given. There was no significant correlation between CCPR and plasma gastrin concentrations, but plasma enteroglucagon concentrations were significantly correlated with CCPR in almost all the sites studied. Plasma PYY concentrations also showed some correlation with CCPR, especially in the colon. Thus while inert bulk cannot stimulate colonic epithelial cell proliferation fermentable fibre is capable of stimulating proliferation in the colon, and especially in the distal colon: it can also stimulate proliferation in the distal small intestine and it is likely that plasma enteroglucagon may have a role to play in this process.

Human colon produces fully processed glucagon‐like peptide‐1 (7–36) amide

“…Whilst the release of GLP-1 by the large intestine has not been demonstrated, this is likely to be the case, given that enteroglucagon and GLP-1 are cosecreted in the ileum [5]. Thus, instillation of glucose [22,23] or fermentable fibre [24] into the colon which stimulate the release of enteroglucagon is likely to also cause GLP-1 secretion. GLP-1 secretion is, therefore, likely to be stimulated by the presence of undigested nutrients in the colon, which occurs in certain pathological conditions in which abnormal amounts of unabsorbed nutrients reach the distal intestine and are associated with elevated concentrations of enteroglucagons [5].…”

The ability of genetically lean or fat slow-growing chickens to synthesize and store lipids is not altered by the dietary energy source

“…Actually, wheat contains soluble NSP affecting all nutrients' digestibility, and particularly the absorption of dietary lipids (Maisonnier et al, 2001). The increase in villi and crypt area observed in the jejunum of chickens fed HL diet could result from the higher level of the poorly fermentable cellulose in this diet compared with LL diet (Goodlad et al, 1987). This could have favored the absorption of dietary lipids in chicken fed this high-fat high fiber diet.…”

A biological function for glucagon-like peptide-2

“…Changes in intestinal epithelial proliferation markers were already evident after a single dose of GLP-2, and morphologic changes were detectable after a treatment period of as little as 4 days (13). Food intake and body weight were similar between control and GLP-2 treated animals, excluding the possibility that increased enteral nutrient ingestion attributable to GLP-2 may have trophic effects on gut epithelium (14).…”

“…As mentioned above, an indirect effect of GLP-2 on gut epithelium by way of increasing food ingestion has been excluded (14). However, GLP-2 treatment has been shown to prevent parenteral nutrition-induced small intestinal hypoplasia in rats.…”