An elemental diet controls inflammation in indomethacin-induced small bowel disease in rats: the role of low dietary fat and the elimination of dietary proteins.

Elemental diets (EDs) are effective in treating Crohn's disease. We hypothesize that low dietary fat and amino acids used as the sole nitrogen source are the major contributors for the success of EDs. We examined the influences of the addition of dietary fat and protein to an ED using an indomethacin-induced inflammation model in rat small intestine. In the ED-fed rats, the intestinal damage score was decreased compared with that in the standard chow group with decreasing intestinal permeability. By supplementing an ED with soybean oil (SO), intestinal permeability was increased to a level similar to that of the standard chow group. For this group, the intestinal damage score also increased compared with that of the ED group but did not reach the levels observed in the standard chow group. The addition of dietary proteins (using heat-denatured pancreatin) resulted in intestinal damage scores that were significantly higher than those of the ED+SO-fed group. The dietary protein increased the intestinal damage score. These results suggest that EDs control inflammation by decreasing intestinal permeability and the elimination of dietary proteins.

Glutamine and arginine affect Caco-2 cell proliferation by promotion of nucleotide synthesis.

OBJECTIVE: We tested our hypothesis that 1) the major effect of Gln is as a nitrogen donor, not an energy source, for nucleotides (NT) and 2) the supplementation of culture medium with arginine (Arg) decreases the flux of glutamine (Gln) for conversion to Arg, thus accelerating NT synthesis. METHODS: Various concentrations of nucleosides (NS+NT) Gln, and glutamate (Glu) in culture were tested for their effect on Caco-2 cell proliferation. (Arg was tested in media with and without Gln to evaluate the Gln pathway. The incorporation of (15)N from L-[5-(15)N]-Gln into NTs of DNA was measured under different NS + NT and Arg concentrations.) RESULTS: The proliferation of Caco-2 cells was increased by NS + NT and Gln supplementation, but not by Glu. The effective concentration of NS + NT was 100-fold smaller than that of Gln. An Arg effect was observed only in the presence of Gln. The NT synthesis from Gln, as indicated by (15)N incorporation from L-[5-(15)N]-Gln, was increased by Arg supplementation and decreased by NS + NT supplementation. CONCLUSION: These results support our hypothesis that the effects of Gln and Arg on Caco-2 cell proliferation are by the promotion of NT synthesis and that the major role of Gln is not energy supply.