‘Luminal Nutrition’ versus ‘Functional Work-Load’ as Controllers of Mucosal Morphology and Epithelial Replacement in the Rat Small Intestine

Abstract

Isotonic solutions of substrate were infused into surgically prepared sacs of upper small intestine in conscious unrestrained rats which fed normally via the gut-in-continuity. Infusion of glucose, galactose or sodium chloride all caused a local increase in villus height, while α-methyl glucoside and mannose had no effect. Glucose, galactose and α-methyl glucoside all stimulated a similar increase in counts of vincristine metaphases in microdissected crypts, although the absolute level of cell production was lower throughout the gut in glucose-infused rats. Sodium chloride infusion also caused a small stimulation of cell production locally, but a considerable increase in the uninfused gut-in-continuity. Mannose infusion had a variable effect on cell production. These results do not support ‘luminal nutrition’ as a controller of epithelial replacement in the rat small intestine, and suggest that a mechanism based on the work-load of the epithelium may be more appropriate.

Regulation of intestinal mucosal growth by amino acids

“…Liquid elemental diets have been reported to cause hyperplasia when infused into bypassed mucosa (Jacobs, et al, 1975). Various sugars, including glucose, have been shown to stimulate cell production when infused into isolated sections of intestine (Clarke RM, 1977). The strongest support for the stimulation of mucosal growth by enteral nutrients has come from experiments involving total parenteral nutrition (TPN), in which glutamine was supplemented enterally or added to the TPN mixture.…”

Enteral nutrition and the small intestine.

“…Deitch has shown that there is a poor correlation between the incidence of translocation and parameters of mucosal mass in rats and mice receiving various enteral and parenteral feeds. 1 16 Further research might be directed at assessing further the benefits of enterotrophic dietary regimens in a clinical setting, with particular attention to the incidence of gut derived sepsis in the critically ill patient, to the efficacy of small intestinal adaptation after gastrointestinal surgery, and to amelioration of cytotoxic or radiation induced intestinal injury. Little is known about the molecular mechanisms that mediate the direct enterotrophic actions of absorbed nutrients, and so research in this field may provide a method of further enhancing mucosal proliferative responses to enteral feeding and of adding to our knowledge of the factors that control epithelial cell growth.…”

Adaptation and carcinogenesis in defunctioned rat colon: Divergent effects of faeces and bile acids

“…The faecal irrigant failed to prevent the loss of weight and length in the TVF, but it did preserve normal crypt depth and it enhanced carcinogenesis. Mechanical stimulation may also be important, since saline irrigation had similar effects; saline alone can stimulate mucosal cell turnover in isolated loops of small bowel (Clarke, 1977). The relative lack of bulk in the irrigant may have facilitated cocarcinogenic activity in other faecal constituents, since it has been suggested that the bulking action of dietary fibre has a protective effect in human large-bowel cancer by reducing exposure of the colonic mucosa to putative faecal carcinogens (Heaton, 1977).…”