Adequate level of carbohydrates in aquafeeds help to conserve protein and reduce cost. However, studies have indicated that high-carbohydrate (HC) diet disrupt the homeostasis of the gut–liver axis in largemouth bass, resulting in decreased intestinal acetate and butyrate level. Herein, we had concepted a set of feeding experiment to assess the effects of dietary sodium acetate (SA) and sodium butyrate (SB) on liver health and the intestinal microbiota in largemouth bass fed an HC diet. The experimental design comprised 5 isonitrogenous and isolipidic diets, including LC (9% starch), HC (18% starch), HCSA (18% starch; 2 g/kg SA), HCSB (18% starch; 2 g/kg SB), and HCSASB (18% starch; 1 g/kg SA + 1 g/kg SB). Juvenile largemouth bass with an initial body weight of 7.00 ± 0.20 g were fed on these diets for 56 d. We found that dietary SA and SB reduced hepatic triglyceride accumulation by activating autophagy (ATG101, LC3B and TFEB), promoting lipolysis (CPT1α, HSL and AMPKα), and inhibiting adipogenesis (FAS, ACCA, SCD1 and PPARγ). In addition, SA and SB decreased oxidative stress in the liver (CAT, GPX1α and SOD1) by activating the Keap1-Nrf2 pathway. Meanwhile, SA and SB alleviated HC-induced inflammation by downregulating the expression of pro-inflammatory factors (IL-1β, COX2 and Hepcidin1) through the NF-κB pathway. Importantly, SA and SB increased the abundance of bacteria that produced acetic acid and butyrate (Clostridium_sensu_stricto_1). Combined with the KEGG analysis, the results showed that SA and SB enriched carbohydrate metabolism and amino acid metabolism pathways, thereby improving the utilization of carbohydrates. Pearson correlation analysis indicated that growth performance was closely related to hepatic lipid deposition, autophagy, antioxidant capacity, inflammation, and intestinal microbial composition. In conclusion, dietary SA and SB can reduce hepatic lipid deposition; and alleviate oxidative stress and inflammation in largemouth bass fed on HC diet. These beneficial effects may be due to the altered composition of the gut microbiota caused by SA and SB. The improvement effects of SB were stronger than those associated with SA.

中文翻译：

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膳食乙酸钠和丁酸钠通过调节大口黑鲈（Micropterus salmoides）的肠道微生物群、肝脏脂质代谢、氧化应激和炎症来提高高碳水化合物饮食的利用率

水产饲料中充足的碳水化合物有助于节省蛋白质并降低成本。然而，研究表明，高碳水化合物（HC）饮食会破坏大口黑鲈肠-肝轴的稳态，导致肠道乙酸和丁酸水平降低。在此，我们构思了一组喂养实验，以评估膳食醋酸钠 (SA) 和丁酸钠 (SB) 对饲喂 HC 饮食的大口黑鲈肝脏健康和肠道微生物群的影响。实验设计包括5种等氮和同脂日粮，包括LC（9%淀粉）、HC（18%淀粉）、HCSA（18%淀粉；2 g/kg SA）、HCSB（18%淀粉；2 g/kg SB）和 HCSASB（18% 淀粉；1 g/kg SA + 1 g/kg SB）。初始体重为 7.00 ± 0.20 g 的幼年大口黑鲈以这些饲料喂养 56 天。我们发现膳食SA和SB通过激活自噬（ATG101、LC3B和TFEB）、促进脂肪分解（CPT1α、HSL和AMPKα）和抑制脂肪生成（FAS、ACCA、SCD1和PPARγ）来减少肝脏甘油三酯积累。此外，SA 和 SB 通过激活 Keap1-Nrf2 通路降低肝脏氧化应激（CAT、GPX1α 和 SOD1）。同时，SA和SB通过NF-κB通路下调促炎因子（IL-1β、COX2和Hepcidin1）的表达，从而减轻HC诱导的炎症。重要的是，SA 和 SB 增加了产生乙酸和丁酸盐的细菌的丰度 (Clostridium_sensu_stricto_1)。结合KEGG分析结果显示，SA和SB丰富了碳水化合物代谢和氨基酸代谢途径，从而提高了碳水化合物的利用率。 Pearson相关分析表明，生长性能与肝脏脂质沉积、自噬、抗氧化能力、炎症和肠道微生物组成密切相关。综上所述，膳食SA和SB可以减少肝脏脂质沉积；并减轻以 HC 饮食喂养的大口黑鲈的氧化应激和炎症。这些有益作用可能是由于 SA 和 SB 改变了肠道微生物群的组成。 SB的改善效果强于SA。