Ge Xiaoyuan, Pan Jintao, Deng Junming, Mai Kangsen, Zhang Yanjiao
Key Laboratory of Aquaculture Nutrition and Feed, Ministry of Agriculture, The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, China.
Laboratory of Aquatic Animal Nutrition and Feed, Fisheries College, Guangdong Ocean University, Zhanjiang, 524088, China.
Fish Shellfish Immunol. 2025 Sep 3;167:110699. doi: 10.1016/j.fsi.2025.110699.
This study investigated the protective effects of dietary niacin on the intestinal health of juvenile turbot fed a high-lipid diet (HLD). Two isonitrogenous and isolipidic diets were formulated, including a HLD without niacin addition (HL0) and a HLD supplemented with 80 mg/kg niacin (HL80). Turbot (approximately 13.2 g) were fed two experimental diets for 10 weeks, with each diet assigned to triplicate tanks. Results showed that niacin significantly improved the weight gain rate and specific growth rate of turbot. Dietary niacin significantly down-regulated the expression of toll-like receptors (TLRs), along with their associated signaling components, including myeloid differentiation factor 88 (MyD88), interferon regulatory factor-7 (IRF-7), p38 mitogen-activated protein kinase (p38MAPK), and activator protein-1 (AP-1). This reduction also extended to key molecules in the downstream nuclear factor-kappa B (NF-κB) signaling pathway, such as NF-κB, IκB kinase β (IKKβ), and IκB kinase γ (IKKγ) (P < 0.05). Similarly, niacin supplementation in HLD markedly decreased the gene expression of pro-inflammatory cytokines and the signaling molecule myosin light chain kinase (MLCK), while increasing the expression of anti-inflammatory cytokines, antibacterial peptides, and barrier-enhancing proteins (P < 0.05). Additionally, HLD-induced intestinal oxidative stress was mitigated by niacin supplementation, as demonstrated by the significant upregulation of nuclear factor E2-related factor 2 (Nrf2), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), and heme oxygenase-1 (HO-1) (P < 0.05). Compared with the HL0 group, dietary niacin significantly increased the abundance of short-chain fatty acids (SCFAs)-producing bacteria (Bacteroides, Faecalibacterium, Roseburia, etc.) and lactic acid bacteria (Lactobacillus, Streptococcus, Lactococcus, etc.). In conclusion, these results indicated that dietary niacin could enhance intestinal mucosal immunity, physical barrier function, and antioxidant capacity through coordinated regulation of TLR-MyD88-NF-κB, MLCK, and Nrf2 signaling pathways. Combined with microbial community optimization, this collectively alleviates the negative effects of high-lipid diets on the intestinal health of turbot.
本研究调查了日粮烟酸对高脂日粮（HLD）喂养的幼体大菱鲆肠道健康的保护作用。配制了两种等氮等脂日粮，包括不添加烟酸的HLD（HL0）和添加80mg/kg烟酸的HLD（HL80）。将大菱鲆（约13.2g）投喂两种实验日粮10周，每种日粮分配到三个重复养殖水箱中。结果表明，烟酸显著提高了大菱鲆的增重率和特定生长率。日粮烟酸显著下调了Toll样受体（TLR）及其相关信号成分的表达，包括髓样分化因子88（MyD88）、干扰素调节因子7（IRF-7）、p38丝裂原活化蛋白激酶（p38MAPK）和活化蛋白-1（AP-1）。这种下调还扩展到下游核因子κB（NF-κB）信号通路中的关键分子，如NF-κB、IκB激酶β（IKKβ）和IκB激酶γ（IKKγ）（P<0.05）。同样，在HLD中添加烟酸显著降低了促炎细胞因子和信号分子肌球蛋白轻链激酶（MLCK）的基因表达，同时增加了抗炎细胞因子、抗菌肽和增强屏障蛋白的表达（P<0.05）。此外，添加烟酸减轻了HLD诱导的肠道氧化应激，这通过核因子E2相关因子2（Nrf2）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）、超氧化物歧化酶（SOD）和血红素加氧酶-1（HO-1）的显著上调得到证明（P<0.05）。与HL0组相比，日粮烟酸显著增加了产生短链脂肪酸（SCFA）的细菌（拟杆菌属、粪杆菌属、罗氏菌属等）和乳酸菌（乳杆菌属、链球菌属、乳球菌属等）的丰度。总之，这些结果表明，日粮烟酸可通过协同调节TLR-MyD88-NF-κB、MLCK和Nrf2信号通路来增强肠道黏膜免疫、物理屏障功能和抗氧化能力。结合微生物群落优化，这共同减轻了高脂日粮对大菱鲆肠道健康的负面影响。
