Lu Kang-Le, Xu Wei-Na, Liu Wen-Bin, Wang Li-Na, Zhang Chun-Nuan, Li Xiang-Fei
a Key Laboratory of Aquatic Animal Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology , Nanjing Agricultural University , Number 1 Weigang Road, Nanjing 210095 , China.
J Aquat Anim Health. 2014 Jun;26(2):100-12. doi: 10.1080/08997659.2014.893460.
High-fat diets may have favorable effects on growth, partly based on protein sparing, but high-fat diets often lead to fatty liver (excessive fat deposition in the liver), which may be deleterious to fish growth and health. The goal of this study was therefore to investigate possible adverse effects and how they develop. Juvenile Blunt Snout Bream Megalobrama amblycephala (initial weight ± SE = 17.70 ± 0.10 g) were fed two diets (5% fat [control] or 15% fat). After 8 weeks, fish that were fed the 15% fat diet showed a high rate of mortality and poor growth. The histological results clearly showed that the high fat intake resulted in fat and glycogen accumulation and structural alterations of the hepatocytes, mitochondria, and nuclei. In the high-fat group, impairments of the mitochondria included mitochondrial swelling and the loss of cristae and matrix. Fish that were given the 15% fat diet exhibited low succinate dehydrogenase and Na(+),K(+)-ATPase activities and increased cytochrome-c release from the mitochondria. Expression of genes for complex I and III subunits of the mitochondrial respiratory chain were down-regulated in fish that received the high-fat diet. Increases in malondialdehyde level and the ratio of oxidized glutathione to reduced glutathione suggested oxidative stress in the livers of fish from the high-fat diet group. Moreover, the lower leukocyte count, lysozyme and alternative complement activities, and globulin level in fish that received the high-fat diet indicated suppressive immune responses. Overall, the intake of excessive fat impaired mitochondrial bioenergetics and physiological functions. The dysfunction of the mitochondria subsequently mediated oxidative stress and hepatocyte apoptosis, which in turn led to the reduced efficacy of the immune system.
高脂饮食可能对生长有有利影响，部分基于节省蛋白质，但高脂饮食常导致脂肪肝（肝脏中脂肪过度沉积），这可能对鱼类生长和健康有害。因此，本研究的目的是调查可能的不利影响以及它们如何发展。将团头鲂幼鱼（初始体重±标准误=17.70±0.10克）投喂两种饲料（5%脂肪[对照]或15%脂肪）。8周后，投喂15%脂肪饲料的鱼死亡率高且生长不良。组织学结果清楚地表明，高脂肪摄入导致肝细胞、线粒体和细胞核中脂肪和糖原积累以及结构改变。在高脂组中，线粒体损伤包括线粒体肿胀、嵴和基质丧失。投喂15%脂肪饲料的鱼琥珀酸脱氢酶和Na(+)、K(+)-ATP酶活性降低，线粒体细胞色素c释放增加。高脂饮食组鱼线粒体呼吸链复合体I和III亚基基因的表达下调。丙二醛水平以及氧化型谷胱甘肽与还原型谷胱甘肽的比值增加表明高脂饮食组鱼肝脏存在氧化应激。此外，高脂饮食组鱼白细胞计数、溶菌酶和替代补体活性以及球蛋白水平较低，表明免疫反应受到抑制。总体而言，过量脂肪摄入损害了线粒体生物能量学和生理功能。线粒体功能障碍随后介导了氧化应激和肝细胞凋亡，进而导致免疫系统功效降低。
