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Uridine alleviates high-carbohydrate diet-induced metabolic syndromes by activating sirt1/AMPK signaling pathway and promoting glycogen synthesis in Nile tilapia (Oreochromis niloticus)
Animal Nutrition ( IF 6.1 ) Pub Date : 2023-05-03 , DOI: 10.1016/j.aninu.2023.03.010
Nan-Nan Zhou 1 , Tong Wang 1 , Yu-Xin Lin 1 , Rong Xu 1 , Hong-Xia Wu 1 , Fei-Fei Ding 1 , Fang Qiao 1 , Zhen-Yu Du 1 , Mei-Ling Zhang 1
Affiliation  

Carbohydrates have a protein sparing effect, but long-term feeding of a high-carbohydrate diet (HCD) leads to metabolic disorders due to the limited utilization efficiency of carbohydrates in fish. How to mitigate the negative effects induced by HCD is crucial for the rapid development of aquaculture. Uridine is a pyrimidine nucleoside that plays a vital role in regulating lipid and glucose metabolism, but whether uridine can alleviate metabolic syndromes induced by HCD remains unknown. In this study, a total of 480 Nile tilapia (Oreochromis niloticus) (average initial weight 5.02 ± 0.03 g) were fed with 4 diets, including a control diet (CON), HCD, HCD + 500 mg/kg uridine (HCUL) and HCD + 5,000 mg/kg uridine (HCUH), for 8 weeks. The results showed that addition of uridine decreased hepatic lipid, serum glucose, triglyceride and cholesterol (P < 0.05). Further analysis indicated that higher concentration of uridine activated the sirtuin1 (sirt1)/adenosine 5-monophosphate-activated protein kinase (AMPK) signaling pathway to increase lipid catabolism and glycolysis while decreasing lipogenesis (P < 0.05). Besides, uridine increased the activity of glycogen synthesis-related enzymes (P < 0.05). This study suggested that uridine could alleviate HCD-induced metabolic syndrome by activating the sirt1/AMPK signaling pathway and promoting glycogen synthesis. This finding reveals the function of uridine in fish metabolism and facilitates the development of new additives in aquatic feeds.



中文翻译:

尿苷通过激活 sirt1/AMPK 信号通路和促进尼罗罗非鱼 (Oreochromis niloticus) 的糖原合成来减轻高碳水化合物饮食诱导的代谢综合征

碳水化合物具有节约蛋白质的作用,但由于鱼类对碳水化合物的利用效率有限,长期饲喂高碳水化合物饮食(HCD)会导致代谢紊乱。如何减轻HCD带来的负面影响对于水产养殖业的快速发展至关重要。尿苷是一种嘧啶核苷,在调节脂质和葡萄糖代谢中起着至关重要的作用,但尿苷是否可以缓解HCD诱导的代谢综合征尚不清楚。在本研究中,共有 480 条尼罗罗非鱼(Oreochromis niloticus)(平均初始体重 5.02 ± 0.03 g)喂食 4 种饮食,包括对照饮食 (CON)、HCD、HCD + 500 mg/kg 尿苷 (HCUL) 和 HCD + 5,000 mg/kg 尿苷 (HCUH),持续 8 天周。结果表明,添加尿苷可降低肝脏脂质、血糖、甘油三酯和胆固醇(P  < 0.05)。进一步分析表明,较高浓度的尿苷激活 sirtuin1 ( sirt1 )/腺苷 5-单磷酸激活蛋白激酶 (AMPK) 信号通路,增加脂质分解代谢和糖酵解,同时减少脂肪生成(P  < 0.05)。此外,尿苷增加了糖原合成相关酶的活性(P < 0.05)。本研究表明,尿苷可通过激活sirt1 /AMPK信号通路,促进糖原合成来缓解HCD诱导的代谢综合征。这一发现揭示了尿苷在鱼类代谢中的作用,并促进了水产饲料中新型添加剂的开发。

更新日期:2023-05-03
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