Glycine Alleviated Intestinal Injury by Inhibiting Ferroptosis in Piglets Challenged with Diquat

SIMPLE SUMMARY: Oxidative stress may reduce the growth performance and intestinal health status of weanling piglets. Due to the fact that the body can synthesize glycine, it is generally treated as an amino acid which is nonessential for nourishment. However, previous research has demonstrated that synthesized glycine was unable to support piglets’ newborn growth and development. Moreover, according to several findings, glycine is crucial for relieving oxidative stress and intestinal damage. The purpose of this investigation was to determine whether glycine could lessen the intestinal damage caused by diquat in weanling piglets and the relationship between ferroptosis and diquat-induced intestinal epithelial cell death. The results showed that dietary glycine reduced intestinal oxidative stress induced by diquat in weanling piglets. Furthermore, with increasing anti-oxidative capacity, dietary glycine was able to restrain intestinal epithelial cell ferroptosis triggered by diquat. ABSTRACT: The purpose of this research was to examine the impact of glycine on intestinal injury caused by oxidative stress in piglets. A 2 × 2 factorial experiment with diets (basic diet vs. 1% glycine diet) and oxidative stress (saline vs. diquat) was conducted on 32 weanling piglets. On day 21, all piglets received an injection of either saline or diquat. After 7 days, all pigs were slaughtered and intestinal samples were collected. Dietary glycine supplementation improved intestinal mucosal morphology, increased the activities of disaccharidases and enhanced intestinal mucosal antioxidant capacity, while regulating the expression of ferroptosis mediators in the piglets under oxidative stress. These findings suggested that dietary glycine supplementation improved the morphology and function of the intestinal mucosa, which was involved in regulating antioxidant capacity and ferroptosis.