Glutamine alleviates bisphenol A-induced jejunal injury in piglets involving mitochondrial function restoration and AMPK-mTOR signaling regulation.

Bisphenol A (BPA), an extensively distributed environmental pollutant, disrupts intestinal homeostasis and promotes epithelial injury in piglets. A vital energy substrate for intestinal epithelial cells, glutamine (Gln) is essential for preserving intestinal barrier function and promoting epithelial restoration. However, the mechanisms underlying the protective effects of Gln against BPA-induced intestinal injury remain incompletely understood. Therefore, piglet and porcine intestinal epithelial cell models were used to investigate the protective effects of Gln and its potential regulatory mechanisms during BPA exposure.The results revealed that BPA exposure impaired intestinal morphology and barrier integrity, accompanied by reduced tight junction protein expression, decreased epithelial renewal capacity, altered JNK/MAPK signaling responses, and disrupted mitochondrial structure and energy metabolism. In contrast, Gln supplementation markedly alleviated BPA-induced jejunal injury, which was associated with improved mitochondrial function and altered AMPK-mTOR signaling activity.Collectively, these findings suggest that Gln supplementation protects against BPA-induced jejunal injury in piglets, potentially through improving mitochondrial metabolic homeostasis and modulating AMPK-mTOR signaling responses. This study provides evidence supporting the potential application of Gln as a nutritional strategy for maintaining intestinal function under environmental stress.