Salidroside Promotes Fatty Acid β-Oxidation and Reduces Hepatic Lipid Deposition in Largemouth Bass by Activating Autophagy via the AMPK/mTOR Pathway

Replacing expensive fishmeal with economically viable plant-derived carbohydrates in aquafeeds holds significant promise. However, excess dietary carbohydrates can induce hepatosteatosis in fish. This study investigated the effects of salidroside (Sal) supplementation of high-carbohydrate (HC) diets on the growth, hepatic fatty acid oxidation, and lipid metabolism of largemouth bass, Micropterus salmoides. Sal did not enhance growth performance but significantly ameliorated morphological indices in HC-fed fish and markedly reduced hepatic triglycerides (TGs), enhanced lipolysis, and stimulated β-oxidation of fatty acids. Furthermore, Sal significantly upregulated AMPKα phosphorylation while downregulating mTOR phosphorylation, thereby activating autophagy-related gene expression. Pearson correlation analysis indicated a strong association between reduced lipid deposition and the AMPK/mTOR-mediated activation of autophagy. In vitro experiments confirmed that Sal activates autophagy via the AMPK/mTOR pathway, thereby mitigating the high-glucose-induced accumulation of TGs. Thus, Sal alleviates hepatic lipid deposition in largemouth bass by activating the AMPK/mTOR signaling pathway, inducing autophagy, and promoting β-oxidation of fatty acids. This study provides evidence for Sal's therapeutic potential against piscine fatty liver disease and identifies novel targets for managing pathological lipid deposition in aquaculture species.