High-fat diet (HFD) usually induces oxidative stress and astaxanthin is regarded as an excellent anti-oxidant. An 8-week feeding trial was conducted to investigate the effects of dietary astaxanthin supplementation on growth performance, lipid metabolism, antioxidant ability, and immune response of juvenile largemouth bass (Micropterus salmoides) fed HFD. Four diets were formulated: the control diet (10.87% lipid, C), high-fat diet (18.08% lipid, HF), and HF diet supplemented with 75 and 150 mg kg⁻¹ astaxanthin (HFA1 and HFA2, respectively). Dietary supplementation of astaxanthin improved the growth of fish fed HFD, also decreased hepatosomatic index and intraperitoneal fat ratio of fish fed HFD, while having no effect on body fat. Malondialdehyde content and superoxide dismutase activity were increased in fish fed HFD, astaxanthin supplementation in HFD decreased the oxidative stress of fish. The supplementation of astaxanthin in HFD also reduced the mRNA levels of Caspase 3, Caspase 9, BAD, and IL15. These results suggested that dietary astaxanthin supplementation in HFD improved the growth performance, antioxidant ability and immune response of largemouth bass.

Dietary bile acid (BA) supplementation can notably ameliorate fatty liver disease caused by high dietary lipids, but the mechanism behind this is poorly understood. The present study was aimed at gaining insight into how TCA (taurocholic acid sodium) reduced hepatic lipid accumulation via the regulation of bile acid metabolism. We explored BA metabolism in juvenile hybrid grouper (Epinephelus fuscoguttatus♀ × E. lanceolatus♂). Three trials were: (1) fed the control, high lipid (HD) or gradient TCA diet; (2) fed a BA diet with or without antibiotics; and (3) injected with an agonist or antagonist of TGR5 (G protein-coupled bile acid receptor 1) and FXR (farnesoid X receptor). The results showed that the TCA diet (about 900 mg kg⁻¹) significantly reduced lipid accumulation in the liver, thus improving liver health. The HD suppressed the abundance of bile-salt hydrolase (BSH) microbes, thus decreasing the concentration of unconjugated primary BAs. TCA administration altered the gut microbial composition and weakened the effects of the HD, thus increasing the level of unconjugated BAs. TCA treatment increased the transport and reabsorption of BAs by activating the TGR5 and FXR signaling pathways, and increased the BA pool size. Furthermore, the presence of microbiota in the intestine increased BA reabsorption and the BA pool size. Our study revealed that exogenous TCA alters the structure of intestinal microbiota and BA composition, then activated the FXR expression, thus regulating the BA metabolism via enhanced BA reabsorption. This, in turn, reduced lipid accumulation and improved the health of the liver in grouper.