1 Department of Experimental Biology, University of Bologna, Italy, 2 Valle Smarlacca, Ravenna, Italy, 3 Department of Biochemistry, University of Bologna, Italy.
J Fish Dis. 1998 May;21(3):177-84. doi: 10.1046/j.1365-2761.1998.00089.x.
In a comparison of livers in fish (Sparus auratus and Dicentrarchus labrax) feeding on natural sources of food with livers of artificially fed animals, a much higher C18:1/C22:6 ratio was observed in the latter. Staining livers with oil red O showed extensive steatosis in artificially fed fish, but not in those naturally fed. Juvenile artificially fed fish showed a more extensive steatosis and a higher mortality rate. In steatotic fish fed a natural diet for 2 months, the liver exhibited extensive regeneration and only a few steatotic areas remained. Marine teleosts do not appear to have a proliferative response of peroxisomes and this is likely to contribute to liver lipid accumulation and subsequent steatosis. It is suggested that an excess of C18:1 (or other mono-unsaturated fatty acids), coupled with a lack of adaptive peroxisomal proliferation, is the primary cause of lipid droplet formation leading to hepatic steatosis.
在比较以天然食物为食的鱼类(真鲷和斜带石斑鱼)和人工喂养动物的肝脏时,后者的 C18:1/C22:6 比值要高得多。油红 O 染色显示,人工喂养的鱼肝脏有广泛的脂肪变性,但天然喂养的鱼没有。幼鱼人工喂养的鱼表现出更广泛的脂肪变性和更高的死亡率。在脂肪变性的鱼用天然饮食喂养 2 个月后,肝脏表现出广泛的再生,只有少数脂肪变性区域仍然存在。海洋硬骨鱼似乎没有过氧化物酶体的增殖反应,这可能导致肝脏脂质积累和随后的脂肪变性。有人认为,C18:1(或其他单不饱和脂肪酸)过量,加上缺乏适应性过氧化物酶体增殖,是导致肝脂肪变性的脂滴形成的主要原因。