Butyrate is the SCFA responsible for augmenting structural aspects of intestinal adaptations by increasing proliferation and decreasing apoptosis within 4 hours postresection. The intestinotrophic mechanism(s) underlying butyrate's effects may involve GLP-2. Ultimately, butyrate administration may enable an infant with short-bowel syndrome to successfully transition to enteral feedings by maximizing their absorptive area.
The nutritional regulation of intestinal adaptation extends beyond the route of nutrient administration as specific nutrients are known to mediate the adaptive response. Dietary carbohydrates are known to enhance intestinal adaptation in patients with short-bowel syndrome. This review discusses SCFA-induced adaptation in intestinal structure and function in adult rat and neonatal piglet models. Potential mechanisms relate to the salvage of energy as SCFA in the colon, direct mediation of intestinal adaptation by SCFA and stimulated release of glucagon-like peptide-2 (GLP-2) from enteroendocrine L cells by SCFA. Among the produced SCFA, butyrate appears to be responsible for increasing plasma GLP-2 concentration, in addition to the enterotrophic effects. Emerging evidence reveals that physiological concentrations of butyrate acutely upregulate the expression of key enterocyte-associated nutrient transporters. Focused experiments are needed to carefully identify the critical components of intestinal adaptation and yield conclusions regarding the relative contributions of SCFA and GLP-2 during the various phases of this process.
Providing GLP-2 to neonates receiving TPN prevents small intestine atrophy, results in small intestine absorptive capacities that are comparable to when nutrients are provided enterally and may accelerate the transition from TPN to enteral nutrition.
Total parenteral nutrition (TPN) is associated with goblet cell atrophy increasing the risk of bacterial translocation. Butyrate has been shown to enhance mucin production and may be an effective clinical treatment for TPN associated intestinal atrophy. This study assessed the effect of butyrate and short chain fatty acid (SCFA) mixtures on MUC2 expression at transcriptional and translational levels in a short bowel syndrome piglet receiving TPN. Piglets underwent massive small bowel resection and received saline, 9mM butyrate, 60mM butyrate or SCFA mixture parenterally for 12 or 72 hours. Quantitative real time PCR showed an increase in MUC2 expression in 9mM compared to other treatments (p=.04). High iron diamine alcian blue stain revealed a trend increase (p=.102) of sulfated mucins in jejunal villi in 9mM over other groups. MUC2 expression tended to increase over time in the ileum regardless of treatment (p=.069). Augmentation of MUC2 and sulfomucins in the proximal bowel by butyrate supplemented TPN enhances barrier function and decreases the risk of bacterial translocation thereby lending support to the use of butyrate as an efficacious treatment of TPN associated intestinal atrophy.Grant Funding Source: NIDDK 5R01DK057682
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