Lactococcus G423 Improves Lipid Metabolism in Broilers Through the Gut Microbiota-Hepatic Lipid Metabolism Axis

This study aimed to elucidate the role of Lactococcus G423 in regulating the AMPK/PPAR signaling pathway and gut microbiota, and to investigate the mechanisms underlying its potential to improve lipid metabolism in broilers. In this trial, 960 one-day-old Arbor Acres (AA) broilers were randomly assigned to one of three groups: a control group (CON), a low-dose Lactococcus G423 group (Lac-L), and a high-dose Lactococcus G423 group (Lac-H) and each group consists of eight replicates, with 40 individuals per replicate. Compared with the CON group, the Lac-L and Lac-H groups showed no significant differences in ADFI, ADG, FCR, breast muscle yield, leg muscle yield, or abdominal fat yield (P > 0.05). No significant changes were observed in serum TG or LDL levels (P > 0.05). However, the CHO level was significantly decreased (P < 0.05), while the HDL level was significantly increased (P < 0.05). Regarding the AMPK/PPAR signaling pathway, both the Lac-L and Lac-H groups significantly downregulated the hepatic mRNA expression of ACC, FABP1, and MGCR (P < 0.05) while significantly upregulating the expression of APOA1 (P < 0.05) compared to the CON group. Gut microbiota analysis indicated that both treatment groups exhibited significantly increased α-diversity indices (P < 0.05) and altered microbial composition at the family level compared to the CON group. Specifically, the abundances of beneficial families such as Lachnospiraceae and Lactobacillaceae were elevated, while significant changes were observed in other taxa including Ruminococcaceae and Akkermansiaceae (P < 0.05). These changes corresponded with significant differences in the MDI and GMHI (P < 0.05). In conclusion, Lactococcus G423 may regulate lipid metabolism in broilers through the combined modulation of the AMPK/PPAR signaling pathway and the gut microbiota. Specifically, Lactococcus G423 appears to regulate broiler lipid metabolism by modulating the gut microbiota–hepatic lipid metabolism axis.