Early weaning can cause intestinal injury, diarrhea, and even death in piglets, leading to huge economic losses in swine production. Therefore, elucidating the mechanisms underlying weaning-induced intestinal injury is of great importance for effectively alleviating such injury in early-weaned piglets and improving their health and production performance. After weaning, the loss of maternal antibody protection disrupts the intestinal immune system. An increase in intestinal pH and incomplete nutrient digestion following weaning promotes the overgrowth of harmful bacteria, resulting in intestinal microbial dysbiosis. Additionally, weaning stress disrupts the intestinal redox balance, causing an abnormal increase in reactive oxygen and subsequently enhancing apoptosis of intestinal epithelial cells. The appropriate use of feed additives can help maintain intestinal barrier integrity and microbial homeostasis in piglets. Piglets have a high protein requirement for growth; however, high-protein diets with excessive protein levels can cause intestinal dysfunction. Therefore, appropriately reducing dietary protein levels while supplementing with crystalline amino acids may be an effective strategy to alleviate intestinal damage in weaned piglets. Dietary fiber is a nutrient that can improve intestinal function in weaned piglets, primarily by promoting the production of short-chain fatty acids and maintaining microbial homeostasis. Additionally, feed processing can effectively enhance nutrient digestibility and utilization, thereby mitigating intestinal injury caused by solid feed. Here, we synthesize the mechanisms by which weaning induces intestinal injury in piglets and the mitigating effects of various nutritional interventions, aiming to provide a theoretical foundation and practical references for alleviating and treating weaning-associated intestinal damage in piglets.

Tributyrin (TBU) is a good dietary source of butyrate and has beneficial effects on the maintenance of normal intestinal morphology. The present study tested the hypothesis that dietary TBU supplementation could alleviate intestinal injury in the acetic acid (ACA)-induced porcine model of colitis. A total of eighteen piglets (25 d old) were randomly allocated to one of three treatment groups (control, ACA and TBU). The control and ACA groups were fed a basal diet and the TBU group was fed the basal diet supplemented with 0·1 % TBU. On day 15 of the trial, under anaesthesia, a soft catheter was inserted into the rectum of piglets (20–25 cm from the anus), followed by administration of either saline (control group) or ACA (10 ml of 10 % ACA solution for ACA and TBU groups). On day 22 of the trial, after venous blood samples were collected, piglets were killed to obtain mid-ileum and mid-colon mucosae. Compared with the control group, the ACA group exhibited an increase (P< 0·05) in lymphocyte counts, creatinine, PGE2, and malondialdehyde concentrations and diamine oxidase and inducible NO synthase activities in the plasma and lymphocyte density in the colon and a decrease in insulin concentrations and glutathione peroxidase activity, ileal villus height:crypt depth ratios and goblet cell numbers in the colon. These adverse effects of ACA were attenuated by TBU supplementation. Moreover, TBU prevented the ACA-induced increase in caspase-3 levels while enhancing claudin-1 protein and epidermal growth factor receptor (EGFR) mRNA expression in the colonic mucosa. Collectively, these results indicate that dietary supplementation with 0·1 % TBU alleviates ACA-induced intestinal injury possibly by inhibiting apoptosis, promoting tight-junction formation and activating EGFR signalling.