Background
Adequate levels of carbohydrates in aquafeeds help conserve protein and reduce costs. However, studies have shown that a high-carbohydrate (HC) diet disrupts the homeostasis of the gut–liver axis in largemouth bass, resulting in decreased intestinal acetate and butyrate levels. Herein, we assessed the effects of sodium acetate (SA) and sodium butyrate (SB) on liver health and the intestinal microbiota in largemouth bass fed an HC diet. The experimental design comprised five isonitrogenous and isolipid diets, including LC (9% starch), HC (18% starch), HCSA (18% starch; 2 g/kg SA), HCSB (18% starch; 2 g/kg SB), and HCSASB (18% starch; 1 g/kg SA + 1 g/kg SB). Juvenile largemouth bass with an initial body weight of 7.00 ± 0.20 g were reared on the diets for 56 days.
Results
We found that dietary SA and SB reduced hepatic triglyceride accumulation by activating autophagy (ATG101, LC3B, and tfeb), promoting lipolysis (CPT1α, HSL, and AMPKα), and inhibiting adipogenesis (FAS, ACCA, SCD1, and PPARγ). In addition, SA and SB decreased oxidative stress in the liver (CAT, GPX, and SOD) by activating the Keap1-Nrf2 pathway. Meanwhile, SA and SB alleviated HC-induced inflammation by downregulating the expression of pro-inflammatory factors (IL-1β, COX2, Hepcidin1) through the NF-κB pathway. Importantly, SA and SB increased the abundance of bacteria that produce acetic acid and butyrate (Clostridium_sensu_stricto_1). Combined with the KEGG analysis, the results showed that SA and SB enriched carbohydrate metabolism and amino acid metabolism pathways, thereby improving the utilization of carbohydrates. Pearson correlation analysis indicated that growth performance was closely related to hepatic lipid deposition, autophagy, antioxidant capacity, inflammation, and intestinal microbial composition.
Conclusions
In conclusion, dietary SA and SB can reduce hepatic lipid deposition, and alleviate oxidative stress and inflammation in largemouth bass fed an HC diet. These beneficial effects may be due to the altered composition of the gut microbiota caused by SA and SB. The improvement effects of SB were stronger than those associated with SA.