Effects of essential fatty acid-deficient diets on growth, mortality, tissue histopathology and fatty acid compositions in juvenile turbot (Scophthalmus maximus)
Effects of essential fatty acid-deficient diets on growth, mortality, tissue histopathology and fatty acid compositions in juvenile turbot (Scophthalmus maximus)
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DOI：
10.1023/a:1007743532618
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发表时间：
1999-03-01
影响因子：
2.9
通讯作者：
Sargent, JR
中科院分区：
文献类型：
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作者：
Bell, JG;Tocher, DR;Sargent, JR
以鱼油(FO)、亚麻籽油(LO)和橄榄油(OO)三种不同脂肪成分的饲料，分别饲喂初始体重1.2g的大比目鱼幼鱼，饲养12周。与FO(对照组)相比，后两种饲料显著降低了特定生长率，增加了死亡率。在饲喂LO和OO饲料的鱼中，大约一半的鱼有明显的肝脏组织病理学，但在饲喂FO的鱼中，没有发现肝脏组织病理学。病变有细胞改变的迹象，包括浓集的嗜碱性细胞，但没有炎性活动的证据。与饲喂粗脂肪组相比，投喂低氧饲料的鱼体总脂脂肪酸组成增加了18：2N-6和18：3N-3，而降低了所有其他多不饱和脂肪酸(PUFA)的比例，包括生理上重要的20：4N-6、20：5N-3和22：6N-3。与FG组相比，GO组鱼体中几乎2/3的总脂肪酸是单不饱和的，而总饱和脂肪酸和除18：2N-6以外的所有其他PUFA的百分比都显著降低。在肝脏中观察到了对总脂脂肪酸组成的大致相似的影响。与投喂FG的鱼相比，投喂LO的鱼肝脏甘油磷脂中18：2n-6、18：3n-3和20：3n-3的比例显著增加，而C-20和C-22PUFA除20：5n-3外，其余均显著降低。摄食OO的鱼肝脏甘油磷脂的总单不饱和度、18：2N-6、20：2N-6、18：2N-9和20：2N-9显著高于FO组，而20：4N-6和22：6N-3的百分含量显著低于FO组。大脑甘油磷脂对饮食治疗的反应表现出大致相似的变化，尽管脂肪酸变化的幅度小于在肝脏中观察到的变化。与低投喂鱼相比，投喂鱼的死亡率更高，这表明在组织磷脂中掺入18：3N-3比掺入18：1N-9能更有效地抵消长链多不饱和脂肪酸的损失。然而，必须优化饮食中长链多不饱和脂肪酸的水平，以允许正常生长和发育。我们的结论是，缺乏20：5n-3和22：6n-3的饲料并不能上调大比目鱼通过脂肪酸去饱和酶/伸长酶途径的极低通量。
Three diets in which the lipid component was supplied either as fish oil (FO), linseed oil (LO) or olive oil (OO) were fed to duplicate groups of juvenile turbot (Scophthalmus maximus) of initial weight 1.2 g for a period of up to 12 weeks. The latter two diets resulted in a significant reduction in specific growth rate and an increased mortality compared to the FO (control) fed fish. A liver histopathology was evident in around half of the fish fed the LO and OO diets but was absent in fish fed FO. The lesion showed indications of cellular alterations consisting of foci of densely basophilic cells but without evidence of inflammatory activity. The total lipid fatty acid composition of the carcass from fish fed LO had increased percentages of 18:2n-6 and 18:3n-3, but decreased percentages of all other polyunsaturated fatty acids (PUFA) including the physiologically important 20:4n-6, 20:5n-3 and 22:6n-3, compared to fish fed FO. Almost 2/3 of the total fatty acids in the carcass of GO-fed fish were monounsaturated while the percentages of total saturated fatty acids and all other PUFA, except 18:2n-6, were significantly reduced compared to fish fed FG. Broadly similar effects on total lipid fatty acid composition were observed in liver. In the liver glycerophospholipid classes of fish fed LO, percentages of 18:2n-6, 18:3n-3 and 20:3n-3 were significantly increased whereas all C-20 and C-22 PUFA, with the exception of 20:5n-3 in PI, were significantly reduced compared to fish fed FG. The liver glycerophospholipids of fish fed OO all showed significantly increased total monounsaturates, 18:2n-6, 20:2n-6, 18:2n-9 and 20:2n-9 as well as reduced percentages of 20:4n-6 and 22:6n-3, compared to fish fed FO. The brain glycerophospholipids showed broadly similar changes in response to dietary treatment although the magnitude of fatty acid alterations was less than those observed in liver. The greater mortalities in the GO-fed fish compared to the LO-fed fish suggests that incorporation of 18:3n-3 into tissue phospholipids can offset losses of long-chain PUFA more effectively than incorporation of 18:1n-9. However, levels of dietary long-chain PUFA must be optimised to allow normal growth and development. We conclude that the very low flux through the fatty acid desaturase/elongase pathways in turbot is not up-regulated by diets deficient in 20:5n-3 and 22:6n-3.