为探讨高糖饲料对吉富罗非鱼(GIFT Oreochromis niloticus)生长性能、饲料利用和糖脂代谢的影响,设置糖水平为34%的对照饲料(C组,能量水平13.68 k J·g-1)、糖水平为48%的高糖高能饲料(HCE组,能量水平16.03 k J·g-1)和高糖等...为探讨高糖饲料对吉富罗非鱼(GIFT Oreochromis niloticus)生长性能、饲料利用和糖脂代谢的影响,设置糖水平为34%的对照饲料(C组,能量水平13.68 k J·g-1)、糖水平为48%的高糖高能饲料(HCE组,能量水平16.03 k J·g-1)和高糖等能饲料(HE组,能量水平13.81 k J·g-1),在室内循环水系统中饲养初始体质量(20.34±0.42)g的吉富罗非鱼幼鱼60 d。结果表明,HCE组和HE组的增重率、特定生长率、肝脏粗蛋白均显著低于C组(P<0.05),饲料系数、肝脏粗脂肪、肝糖原、总糖表观消化率、血清低密度脂蛋白胆固醇和高密度脂蛋白胆固醇均显著高于C组(P<0.05);HE组增重率、全鱼粗脂肪、血清甘油三酯和总胆固醇均显著低于HCE组(P<0.05);高糖组肝脏葡萄糖激酶显著高于C组,HE组葡萄糖-6-磷酸脱氢酶、苹果酸酶、脂肪酸合成酶活性最高,C组最低(P<0.05);由肝脏组织切片看出,高糖饲料引起吉富罗非鱼肝脏细胞肿大变形,出现空泡,HCE组对肝脏损伤更加显著。研究结果表明,吉富罗非鱼能够耐受48%糖水平的饲料,但长期摄食导致鱼体糖脂代谢紊乱,尤其影响脂肪代谢,造成鱼体脂肪蓄积,肝功能损伤,不利于生长与健康。展开更多
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 neg...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 of480 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.展开更多
目的探讨CD14启动子-159位点C/T多态性对健康青年血脂比值的影响及在高糖低脂(highcarbohydrate/low fat,HC/LF)膳食诱导的血脂比值变化中的作用。方法纳入56名(22.89±1.80岁)健康青年志愿者,先后给予7d平衡膳食和6dHC/LF膳食,于...目的探讨CD14启动子-159位点C/T多态性对健康青年血脂比值的影响及在高糖低脂(highcarbohydrate/low fat,HC/LF)膳食诱导的血脂比值变化中的作用。方法纳入56名(22.89±1.80岁)健康青年志愿者,先后给予7d平衡膳食和6dHC/LF膳食,于第1d、第8d及第14d清晨抽取12h空腹静脉血,测定血脂水平,计算甘油三酯/高密度脂蛋白胆固醇(triglyceride/high density lipoprotein-cholesterol,TG/HDL-c)、log(TG/HDL-c)、总胆固醇/高密度脂蛋白胆固醇(total cholesterol/high density lipoprotein-cholesterol,TC/HDL-c)和低密度脂蛋白胆固醇/高密度脂蛋白胆固醇(low density lipoprotein-cholesterol/high density lipoprotein-cholesterol,LDL-c/HDL-c)。提取基因组DNA,聚合酶链反应-限制性酶切法分析CD14启动子-159位点多态性。结果女性TT纯合子受试者TG/HDL-c(P<0.05),log(TG/HDL-c)(P<0.05)和LDL-c/HDL-c(P<0.05)基础值高于C等位基因携带者,男性C等位基因携带者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.001)和TC/HDL-c(P<0.01)高于女性。HC/LF膳食前,女性TT纯合子受试者TG/HDL-c(P<0.01)、log(TG/HDL-c)(P<0.001)和TC/HDL-c(P<0.05)均高于C等位基因携带者,男性C等位基因携带者4种血脂比值均高于女性(P<0.05)。HC/LF膳食后,女性TT纯合子受试者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.05)和LDL-c/HDL-c(P<0.05)均高于C等位基因携带者,男性C等位基因携带者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.01)高于女性。与HC/LF膳食前相比,HC/LF膳食后男性C等位基因携带者TC/HDL-c(P<0.001)、LDL-c/HDL-c(P<0.01)降低,TT纯合子受试者TC/HDL-c(P<0.001)降低。HC/LF膳食后女性C等位基因携带者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.05)升高,TC/HDL-c(P<0.001)、LDL-c/HDL-c(P<0.01)降低,TT纯合子受试者只有TC/HDL-c(P<0.01)降低。结论相较于T等位基因携带者,C等位基因携带者中,膳食改变对血脂表型的作用是微效,可能被CD14-159位点C等位基因掩盖。HC/LF膳食与CD14-159位点C等位基因的相互作用能够降�展开更多
文摘为探讨高糖饲料对吉富罗非鱼(GIFT Oreochromis niloticus)生长性能、饲料利用和糖脂代谢的影响,设置糖水平为34%的对照饲料(C组,能量水平13.68 k J·g-1)、糖水平为48%的高糖高能饲料(HCE组,能量水平16.03 k J·g-1)和高糖等能饲料(HE组,能量水平13.81 k J·g-1),在室内循环水系统中饲养初始体质量(20.34±0.42)g的吉富罗非鱼幼鱼60 d。结果表明,HCE组和HE组的增重率、特定生长率、肝脏粗蛋白均显著低于C组(P<0.05),饲料系数、肝脏粗脂肪、肝糖原、总糖表观消化率、血清低密度脂蛋白胆固醇和高密度脂蛋白胆固醇均显著高于C组(P<0.05);HE组增重率、全鱼粗脂肪、血清甘油三酯和总胆固醇均显著低于HCE组(P<0.05);高糖组肝脏葡萄糖激酶显著高于C组,HE组葡萄糖-6-磷酸脱氢酶、苹果酸酶、脂肪酸合成酶活性最高,C组最低(P<0.05);由肝脏组织切片看出,高糖饲料引起吉富罗非鱼肝脏细胞肿大变形,出现空泡,HCE组对肝脏损伤更加显著。研究结果表明,吉富罗非鱼能够耐受48%糖水平的饲料,但长期摄食导致鱼体糖脂代谢紊乱,尤其影响脂肪代谢,造成鱼体脂肪蓄积,肝功能损伤,不利于生长与健康。
基金financial support provided by the National Key Research and Development Program(grant number:2022YFD2400800)National Natural Science Foundation of China(grant number:31972798)。
文摘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 of480 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.
文摘目的探讨CD14启动子-159位点C/T多态性对健康青年血脂比值的影响及在高糖低脂(highcarbohydrate/low fat,HC/LF)膳食诱导的血脂比值变化中的作用。方法纳入56名(22.89±1.80岁)健康青年志愿者,先后给予7d平衡膳食和6dHC/LF膳食,于第1d、第8d及第14d清晨抽取12h空腹静脉血,测定血脂水平,计算甘油三酯/高密度脂蛋白胆固醇(triglyceride/high density lipoprotein-cholesterol,TG/HDL-c)、log(TG/HDL-c)、总胆固醇/高密度脂蛋白胆固醇(total cholesterol/high density lipoprotein-cholesterol,TC/HDL-c)和低密度脂蛋白胆固醇/高密度脂蛋白胆固醇(low density lipoprotein-cholesterol/high density lipoprotein-cholesterol,LDL-c/HDL-c)。提取基因组DNA,聚合酶链反应-限制性酶切法分析CD14启动子-159位点多态性。结果女性TT纯合子受试者TG/HDL-c(P<0.05),log(TG/HDL-c)(P<0.05)和LDL-c/HDL-c(P<0.05)基础值高于C等位基因携带者,男性C等位基因携带者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.001)和TC/HDL-c(P<0.01)高于女性。HC/LF膳食前,女性TT纯合子受试者TG/HDL-c(P<0.01)、log(TG/HDL-c)(P<0.001)和TC/HDL-c(P<0.05)均高于C等位基因携带者,男性C等位基因携带者4种血脂比值均高于女性(P<0.05)。HC/LF膳食后,女性TT纯合子受试者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.05)和LDL-c/HDL-c(P<0.05)均高于C等位基因携带者,男性C等位基因携带者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.01)高于女性。与HC/LF膳食前相比,HC/LF膳食后男性C等位基因携带者TC/HDL-c(P<0.001)、LDL-c/HDL-c(P<0.01)降低,TT纯合子受试者TC/HDL-c(P<0.001)降低。HC/LF膳食后女性C等位基因携带者TG/HDL-c(P<0.05)、log(TG/HDL-c)(P<0.05)升高,TC/HDL-c(P<0.001)、LDL-c/HDL-c(P<0.01)降低,TT纯合子受试者只有TC/HDL-c(P<0.01)降低。结论相较于T等位基因携带者,C等位基因携带者中,膳食改变对血脂表型的作用是微效,可能被CD14-159位点C等位基因掩盖。HC/LF膳食与CD14-159位点C等位基因的相互作用能够降�
