Species specificity of arginine deficiency-induced hepatic steatosis.
Species specificity of arginine deficiency-induced hepatic steatosis.
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精氨酸缺乏引起的肝脂肪变性的物种特异性。
DOI：
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发表时间：
1981
期刊：
影响因子：
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通讯作者：
A. S. Hassan
中科院分区：
文献类型：
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作者：
J. Milner;A. S. Hassan
发现大鼠食用缺乏精氨酸的饮食导致的肝脏脂肪变性与年龄或大小无关。脂质生物合成的速率，如在体外掺入的14 C-乙酸酯显着增加，在大鼠喂养的精氨酸缺乏的饮食时，表示每毫克肝脏。补充精氨酸缺乏的饮食与1%核糖，1%次黄嘌呤或0.2%腺嘌呤抑制精氨酸缺乏引起的脂肪浸润。补充肌苷、黄嘌呤或尿嘧啶对精氨酸缺乏引起的脂肪浸润、肝乳清酸生物合成或尿乳清酸排泄无显著影响。在喂食无精氨酸饲料的小鼠、仓鼠和家兔中也观察到乳清酸排泄增加。然而，连续21天食用缺乏精氨酸的饮食并没有显着改变小鼠、仓鼠或兔子的肝脏脂质含量。虽然脂肪浸润似乎仅限于大鼠，但在喂食缺乏精氨酸的饲料的大鼠、仓鼠和家兔中观察到肝脏核苷酸改变。精氨酸缺乏症和乳清酸喂养在各种物种的相似性进行了讨论。
Hepatic steatosis resulting from the consumption of an arginine-deficient diet in the rat was found to occur independent of age or size. The rate of lipid biosynthesis as indicated by in vitro incorporation of 14C-acetate was significantly increased in rats fed an arginine-deficient diet when expressed per milligram liver. Supplementation of the arginine-deficient diet with 1% ribose, 1% hypoxanthine or 0.2% adenine depressed the fatty infiltration caused by arginine deficiency. Inosine, xanthine or uracil supplementation did not significantly alter the fatty infiltration, liver orotic acid biosynthesis or urinary orotic excretion induced by the arginine deficiency. Increased orotic acid excretion was also observed in the mouse, hamster and rabbit fed a diet devoid of arginine. However, consumption of the, arginine-deficient diet for 21 days did not significantly alter the liver lipid content of mice, hamsters or rabbits. Although the fatty infiltration appears to be limited to the rat, altered liver nucleotides were observed in rats, hamsters and rabbits fed an arginine-deficient diet. Similarities of arginine deficiency and orotic acid feeding in various species are discussed.