Lecithin supplementation to HFD improves largemouth bass liver health: Implications for regulating lipid homeostasis, antioxidant responses and endoplasmic reticulum stress.

Dietary lipids serve as economical energy sources in aquaculture feeds. Elevating lipid content promotes protein conservation and mitigates nitrogen waste. Fish health, however, can be severely impacted by fatty liver resulting from prolonged high-fat diet (HFD) feeding. Adding lecithin to the feed might be a potential improvement solution. This study investigated how dietary lipid and phospholipid levels affect hepatic lipid homeostasis, endoplasmic reticulum (ER) stress, and redox balance in largemouth bass. Five diets were formulated: a control (10.67% lipid, no added lecithin), a normal-lipid diet with 1.0 g/kg lecithin, the HFD (18.65% lipid, no added lecithin), and the HFD supplemented with either 1.0 or 2.0 g/kg lecithin (HFD + lecithin 1, HFD + lecithin 2). Lecithin supplementation reversed HFD-induced intrahepatic fat deposition while mitigating the decline in hepatic polyunsaturated fatty acids content. Lecithin supplementation mitigated HFD-stimulated increases in hepatic triglyceride, total cholesterol, key lipogenic enzyme activities, and mRNA levels of lipogenic genes/transcription factors. Furthermore, lecithin lessened the impact of HFD on hepatic very low density lipoprotein (VLDL), preventing both a lessened VLDL content and diminished VLDL secretion. Regarding ER stress and antioxidant responses: dietary lecithin addition alleviated HFD-induced increment of mRNA levels of ER stress markers and MDA content, and mitigated HFD-induced reduction of hepatic total superoxide dismutase, catalase, and total antioxidant capacity. This demonstrates lecithin's protective role against HFD-induced hepatic injury by restoring lipid homeostasis, alleviating ER stress, and strengthening antioxidant capacity.