饲料中高浓度N-氨甲酰谷氨酸对罗非鱼脂肪代谢的影响

THE EFFECT OF HIGH DIETARY N-CARBAMYLGLUTAMATE CONTENTS ON LIPID METABOLISM

  • 摘要: 本实验旨在研究饲料中添加高浓度N-氨甲酰谷氨酸(NCG)对罗非鱼(Oreochromis niloticus)鱼体脂肪含量、血清生化指标、肝脏脂肪沉积、脂肪代谢基因表达的影响。选取360尾平均体质量为(32.56±1.12) g的罗非鱼, 随机分为3组, 每组设置3个重复, 每个重复40尾鱼。以不添加NCG组的基础饲料作为对照, 另外设置添加高浓度2000和5000 mg/kg NCG的2种实验饲料作为实验组(NCG I和NCG II)。每天按体重4%定量投喂2次, 共饲养8周。研究结果表明, 高浓度NCG添加水平升高了罗非鱼的肝体指数, NCG II组的肝体指数显著增加(P<0.05)。NCG I和NCG II组罗非鱼血清甘油三酯和胆固醇含量显著高于对照组(P<0.05), 且NCG II组罗非鱼血清的谷丙转氨酶和谷草转氨酶的活性显著升高(P<0.05)。高浓度NCG的添加显著提高罗非鱼内脏脂肪含量, 并显著减少内脏蛋白质含量(P<0.05)。肝脏HE染色和油红O染色结果显示, 高浓度NCG添加组的肝脏细胞出现了空泡化变性和明显的脂滴富集现象, 且NCG II组比NCG I组的罗非鱼肝脏中的空泡更大, 脂滴更大更集中。在进食高浓度NCG后, 罗非鱼肝脏中脂肪氧化分解相关基因肉碱棕榈酰转移酶1基因(Carnitine palmitoyl transferase 1)、基因过氧化物酶体增殖物激活受体a基因(Peroxisome proliferator activated receptor alpha)和解偶联蛋白1基因(Uncoupling protein 1)的表达量显著降低(P<0.05)。综上, 高浓度NCG的添加会造成罗非鱼的脂肪代谢异常, 使得血脂升高, 并诱导出严重脂肪肝症状和内脏脂肪蓄积, 这可能是高浓度NCG降低了肝脏脂肪β-氧化相关基因的表达所导致。

     

    Abstract: The aim of this study was to investigate the effects of high dietary N-carbamylglutamate (NCG) contents on serum biochemical indicators, liver fat deposition, body fat content, and fat metabolism genes expression in tilapia (Oreochromis niloticus). Tilapia of 360 with an average body mass of (36.56±1.12) g were divided into 3 groups, each with 3 replicates containing 40 fish per replicate. The control group received basic feed without the addition of NCG, while two experimental groups received feed supplemented with high concentrations of 2000 and 5000 mg/kg NCG, respectively. The tilapia were fed twice daily at a rate of 4% body weight. After 8 weeks, the addition of high dietary NCG contents increased the hepatosomatic index of tilapia, with the hepatosomatic index of the NCG II group significantly increased (P<0.05). Liver histological analysis using HE-staining and oil red O-staining showed vacuolar degeneration and significant lipid droplet accumulation in liver cells of the high concentration NCG addition group. Moreover, the tilapia liver in the NCG II group exhibited larger vacuoles and more concentrated lipid droplets compared to the NCGI group. High concentration NCG addition significantly increased the visceral fat content of tilapia while significantly reducing visceral protein content (P<0.05). Serum triglycerides and cholesterol levels in the NCG I and NCG II groups were significantly higher than those in control group (P<0.05). Furthermore, the activities of alanine aminotransferase and aspartate aminotransferase in tilapia serum were significantly increased in the NCG II group (P<0.05). Consumption of high concentrations of NCG led to a significant decrease in the expression levels of genes related to lipid oxidation and decomposition in tilapia liver (P<0.05), including carnitine palmitoyltransferase 1 (cpt1), peroxisome proliferator activated receptor a (ppara), and uncoupling protein 1 (ucp1). In summary, the addition of high dietary NCG contents caused abnormal fat metabolism in tilapia, leading to elevated serum triglycerides and inducing severe symptoms of fatty liver. This effect may be attributed to the decrease in gene expression related to liver fatty acid β-oxidation caused by high dietary NCG contents.

     

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