Glycerol monolaurate attenuates necrotic enteritis in broilers by improving gut–liver health and remodeling the gut microbiota

BACKGROUND: Necrotic enteritis (NE) is a widespread avian intestinal disease that causes substantial economic losses in poultry production. With increasing restrictions on antibiotic use, sustainable alternatives are urgently needed. Glycerol monolaurate (GML) has anti-inflammatory and antimicrobial properties, but its role in preventing NE remains unclear. This study aimed to investigate the protective effects of GML on gut-liver health and the cecal microbiota in NE-challenged broilers. RESULTS: A total of 288 broilers were fed diets supplemented with 1,200 mg/kg GML for 21 d under an NE challenge model. GML improved the average daily gain and jejunal villus height while reducing the intestinal lesion score in NE broilers (P < 0.05). GML upregulated the expression of the tight junction genes OCLN and MUC2 and downregulated the expression of the proinflammatory cytokines interleukin (IL)-1β, IL-8, and tumor necrosis factor (TNF)-α, as well as RELA and IRF5 (P < 0.05). Moreover, GML reduced endotoxin levels and alleviated oxidative stress in the jejunum of NE broilers. NE infection increases intestinal permeability, resulting in elevated serum proinflammatory cytokine (IL-1β, TNF-α) and intestinal-derived endotoxin levels, which subsequently contribute to liver injury. GML significantly alleviated this liver damage, as evidenced by reduced hepatic steatosis and lower serum alanine aminotransferase levels (P < 0.05). Furthermore, GML relieved the NE-induced increase in serum endotoxin and proinflammatory cytokine levels and improved the hepatic antioxidant status by decreasing the malondialdehyde content and increasing superoxide dismutase activity (P < 0.05). Additionally, GML significantly enhanced the alpha diversity indices and increased the relative abundances of Parabacteroides, Lactobacillus, Blautia, and DTU089 in the ceca of NE broilers, with these microbial changes showing significant correlations with improvements in inflammatory and oxidative status. GML altered microbial functions in NE broilers, affecting pathways related to the biosynthesis of unsaturated fatty acids, antibiotic biosynthesis, and phosphonate and phosphinate metabolism. These functional shifts support the potential mechanisms through which the altered microbiota may contribute to the observed improvements. CONCLUSIONS: In summary, GML supplementation alleviated NE in broilers by enhancing intestinal barrier function, reducing inflammation and oxidative stress, and modulating the gut microbiota composition, thereby attenuating gut-derived liver injury and improving growth performance.