Inhibited autophagy impairs systemic nutrient metabolism in Nile tilapia

Autophagy is a conserved cellular degradation process through which intracellular components are degraded by the lysosome, but its roles in fish metabolism have not been studied in depth. Therefore, the present study aimed to investigate whether autophagy plays a key role in maintaining metabolic homeostasis in fish. In an 8-week feeding trial, Nile tilapia were fed either a control diet with medium fat and medium carbohydrate (Control), or a control diet supplemented with a classic autophagy inhibitor (chloroquine, CQ). CQ supplementation significantly inhibited autophagy and impaired fish growth and protein synthesis, and the glycolysis was stimulated, accompanied by fat accumulation, high oxidative stress and inflammation. Physiological status and gene expressions suggested that impaired autophagy might be at least one cause of the metabolic diseases which has been commonly seen in aquaculture. These results indicate that inhibition of autophagy could significantly affect the metabolism of lipid, carbohydrate and protein in fish; hence, autophagy could play important roles in maintaining homeostasis of nutrient metabolism in cultured fish. [Display omitted] •Chloroquine supplementation significantly inhibited autophagy and impaired the growth of Nile tilapia.•Autophagy inhibition could cause lipid accumulation and have adverse impacts on lipid metabolism.•Autophagy inhibition tended to stimulate glucose metabolism but reduce protein synthesis.•Autophagy inhibition could induce oxidative stress and inflammation.