Rashwan Aya G, Assar Doaa H, Salah Abdallah S, Abualreesh Muyassar H, Salem Shimaa M R, Althobaiti Norah, Elbialy Zizy I
Faculty of Aquatic and Fisheries Sciences, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt.
Clinical Pathology Department, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt.
Sci Rep. 2025 Jan 10;15(1):1581. doi: 10.1038/s41598-024-84814-1.
This study was performed to reveal the metabolic effects and molecular mechanisms that govern the dietary incorporation of clenbuterol on growth performance, haemato-biochemical changes, histological alteration, and gene expression regulating glucose and lipid metabolism in normal and high-fat diets fed in Nile tilapia (Oreochromis niloticus). Six experimental diets were formulated, incorporating different concentrations of clenbuterol. The 1st three groups were supplemented with a diet comprising 6% fat, with clenbuterol of 0, 5, and 10 g/kg diet was designated as F6 clenb0, F6clenb5, and F6clenb10, respectively. The other treatment groups were fed a diet of 12% fat, with clenbuterol 0, 5, and 10 g/kg diet, respectively termed F12 clenb0, F12 clenb5, and F12 clenb10. The results revealed that compared to the control group, HFD exhibited a marked reduction in FBW, BWG, PER, and body protein percent but significantly increased the FCR, IPF, liver fat percent, and body ash percent with altered hematological parameters, raised serum biomarkers of hepatic and renal injury. HFD signally raised mRNA expression of pro-inflammatory cytokines, and declined nrf2 and antioxidative function-related genes. Also increased mRNA expression of lipogenic genes as FAS and SREBP-1c and gluconeogenic genes as pepck and g6pc while downregulated, pparα, cpt1, acox1. Nevertheless, clenbuterol supplementation significantly reversed the aforementioned findings induced by HFD. Clenbuterol inclusion significantly improves growth performance and antioxidant defenses by modulating nrf2 signaling and reducing inflammatory response, reduces fatty acid synthesis, and enhances mitochondrial β-oxidation not only functioning as a lipid regulator and effectively alleviating fat accumulation in the liver but playing an essential role in the control of glucose metabolism by reducing hepatic glucose production in high-fat diet-fed Nile tilapias well.
本研究旨在揭示克伦特罗掺入饲料对尼罗罗非鱼(Oreochromis niloticus)生长性能、血液生化变化、组织学改变以及调节正常和高脂饲料中葡萄糖和脂质代谢的基因表达的代谢影响和分子机制。配制了六种实验饲料,其中包含不同浓度的克伦特罗。前三组补充含6%脂肪的饲料,克伦特罗添加量分别为0、5和10 g/kg饲料,分别命名为F6 clenb0、F6clenb5和F6clenb10。其他处理组饲喂含12%脂肪的饲料,克伦特罗添加量分别为0、5和10 g/kg饲料,分别称为F12 clenb0、F12 clenb5和F12 clenb10。结果显示,与对照组相比,高脂饲料组的终末体重、增重、蛋白质效率和体蛋白百分比显著降低,但饲料系数、肝体指数、肝脂肪百分比和体灰分百分比显著升高,血液学参数改变,肝脏和肾脏损伤的血清生物标志物升高。高脂饲料显著上调促炎细胞因子的mRNA表达,降低核因子E2相关因子2(nrf2)和抗氧化功能相关基因的表达。同时,脂肪酸合成酶(FAS)和固醇调节元件结合蛋白-1c(SREBP-1c)等脂肪生成基因以及磷酸烯醇式丙酮酸羧激酶(pepck)和葡萄糖-6-磷酸酶(g6pc)等糖异生基因的mRNA表达增加,而过氧化物酶体增殖物激活受体α(pparα)、肉碱/有机阳离子转运体1(cpt1)、酰基辅酶A氧化酶1(acox1)表达下调。然而,补充克伦特罗显著逆转了高脂饲料诱导的上述结果。添加克伦特罗通过调节nrf2信号通路和减轻炎症反应,显著改善生长性能和抗氧化防御能力,减少脂肪酸合成,增强线粒体β-氧化,不仅作为脂质调节剂发挥作用,有效减轻高脂饲料喂养的尼罗罗非鱼肝脏中的脂肪积累,而且在通过减少肝脏葡萄糖生成来控制葡萄糖代谢方面也发挥着重要作用。