Mechanism of Lactococcus lactis L19 in alleviating high-carbohydrate diet-induced glucose and lipid metabolism disorders in northern snakehead (Channa argus).

To reduce the adverse effects of high-carbohydrate diets (HC diets), this study aimed to investigate the mechanisms of the regulatory effects of supplementation of the HC diets with the snakehead homolog Lactococcus lactis L19 (L. lactis L19) on growth performance, oxidative stress, inflammation, glucose and lipid metabolism, and apoptosis in Channa argus (C. argus). A total of 270 fish were divided into control (CON), HC, and HC supplemented with 1 × 108 CFU/g L. lactis L19 (HL19) groups and fed for 8 weeks. Results showed that L19 enhanced growth performance and insulin secretion while reducing blood glucose and blood lipids. Liver H&E and PAS staining showed that supplementation with L19 ameliorated HC diet-induced liver damage and glycogen accumulation. Simultaneously, L19 promoted glycolysis and gluconeogenesis enzyme activities and gene expression, inhibited ACC and FAS, and promoted CPT1 and HSL; L19 also reduced the content of oxidative stress parameters and increased the activities of antioxidant enzymes and related gene expression levels (nrf2, ho-1, and nqo-1), thereby alleviating oxidative stress; furthermore, L19 enhanced serum immunological parameters and mitigated inflammation and apoptosis by upregulating anti-inflammatory factors (tgf-β, il-10, iκbα, and il-1β), anti-apoptotic gene bcl2, and heat shock proteins (hsp70 and hsp90) and downregulating the expressions of pro-inflammatory factors (nf-κb, tnf-α, il-8, and il-6) and pro-apoptotic genes (cas3, cas8, cas9, and bax). In conclusion, L19 supplementation enhanced the growth performance in C. argus by activating the IR/PI3K/AKT pathway, thereby ameliorating the glucose and lipid metabolism disorders induced by HC diets, effectively alleviating oxidative stress, inhibiting inflammation, and preventing apoptosis.