Alginate Oligosaccharide-induced Intestinal Morphology, Barrier Function and Epithelium Apoptosis Modifications Have Beneficial Effects on the Growth Performance of Weaned Pigs

Background: Alginate oligosaccharide (AOS), produced from alginate by alginate lyase-mediated depolymerisation, is a potential substitute for antibiotics and possesses growth-enhancing effects. Nevertheless, the mechanisms by which AOS regulates porcine growth remain to be elucidated. Therefore, we investigated the AOS-mediated changes in the growth performance of weaned pigs by determining the intestinal morphology, barrier function, as well as epithelium apoptosis.

Methods: Twenty-four weaned pigs were distributed into two groups ( = 12) and received either a basal diet (control group) or the same diet supplemented with 100 mg/kg AOS. On d 15, -xylose (0.1 g/kg body weight) was orally administrated to eight randomly selected pigs per treatment, and their serum and intestinal mucosa samples were collected 1 h later.

Results: Our results showed that inclusion of AOS in the diet for 2 wk increased ( < 0.05) the average daily body weight gain in weaned pigs. Notably, AOS supplementation ameliorated the intestinal morphology and barrier function, as suggested by the enhanced ( < 0.05) intestinal villus height, secretory immunoglobulin A content and goblet cell counts. Compared to the control group, AOS ingestion both decreased ( < 0.05) the total apoptotic percentage and increased ( < 0.05) the proportion of S phase in the intestinal epithelial cells. Furthermore, AOS not only up-regulated ( < 0.05) the B-cell lymphoma-2 () transcriptional level but also down-regulated ( < 0.05) the B-cell lymphoma-2-associated X protein (), cysteinyl aspartate-specific proteinase-3 () and transcriptional levels in the small intestine.

Conclusions: In summary, this study provides evidence that supplemental AOS beneficially affects the growth performance of weaned pigs, which may result from the improved intestinal morphology and barrier function, as well as the inhibited enterocyte death, through reducing apoptosis via mitochondria-dependent apoptosis.