cysteinylglycine and alanylalanine

PepT1, a di/tripeptide transporter, is preferentially preserved over free amino acid transporters in situations of gut stress. Therefore, our objective was to determine the impact of enterally delivered dipeptide-containing diets on indices of intestinal adaptation in neonatal piglets after intestinal resection.. Piglets (n = 25, 10 ± 1 d old) underwent an 80% jejuno-ileal resection and were provided 50% of nutritional support as TPN, and 50% as one of five, enteral test diets: 1) a control diet containing free amino acids, or the same diet but with equimolar amounts of free amino acids replaced by 2) alanyl-alanine, 3) alanyl-glutamine, 4) cysteinyl-glycine, or 5) both alanyl-alanine and cysteinyl-glycine. After 4 d of enteral feeding, indices of intestinal adaptation were assessed. Outcome measures included plasma and mucosal amino acid concentrations, morphological and histological parameters, protein synthesis, PepT1 mRNA and protein expression, and mucosal cytokine concentrations.. Intestinal length, organ weight and protein synthesis rates were not different amongst groups. All of the dipeptide-containing diets reduced pro-inflammatory cytokine concentrations in the mucosa (TNF-α, IFN-γ). The cysteinyl-glycine diet supported greater villus height compared to all other dipeptides and greater crypt depth compared to alanyl-glutamine; however, none of the dipeptide diets altered intestinal morphology compared to the free amino acid control diet.. This study showed that while there was no explicit morphological benefit of enteral dipeptides over their constituent free amino acids, there was the potential for the amelioration of intestinal inflammation by reducing pro-inflammatory cytokines. Enteral provision of dipeptides impacted intestinal adaptation, but the response was dipeptide-specific.

Topics: Animals; Dipeptides; Disease Models, Animal; Enteral Nutrition; Glutathione; Inflammation; Interferon-gamma; Intestine, Small; Organ Size; Swine; Treatment Outcome; Tumor Necrosis Factor-alpha