Abstract

A high-fat diet can lead to fat deposition in the liver. Astaxanthin is reported to exert a hepatoprotective effect by affecting host fat metabolism. However, the molecular mechanism used by astaxanthin to regulate fat metabolism is still unclear. This study aimed to examine the function and molecular mechanism used by astaxanthin-enriched Oedocladium sp. in attenuating liver damage and fat deposition that was caused by a high-fat diet. The normal-fat diet (NF), high-fat diet (HF), and high-fat diet supplemented with Oedocladium sp. (HFO) were used to feed juvenile Trachinotus ovatus for 8 weeks. The findings of this study indicated that the HFO diet mitigated growth decline caused by the HF diet by improving digestibility and feed utilization. Meanwhile, the HFO diet reduced serum cholesterol and triglycerides as well as hepatic fat accumulation, alleviating inflammation, oxidative stress, and immunosuppression caused by an HF diet. Additionally, the HFO diet activated AMPK/ACC/CPT1 signal and suppressed the AMPK/SREBP1/FAS signal to promote the catabolism and transport of fat molecules and inhibit fat synthesis. This was regarded as an important regulatory mechanism that was used by Oedocladium sp. to alleviate the fat deposition induced by an HF diet. AMPK may be a key target for Oedocladium sp. to regulate fat metabolism. Therefore, Oedocladium sp., a promising source of astaxanthin, can be used in HF diets to enhance the health and productivity of farmed fish.

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