Milner J A
J Nutr. 1979 Apr;109(4):663-70. doi: 10.1093/jn/109.4.663.
Arginine deficiency is known to lead to marked alterations in pyrimidine biosynthesis and the excessive loss of urinary orotic acid. Orotic acid feeding is known to lead to hepatic steatosis. These studies show that arginine deficiency also results in a marked increase in liver lipids in the rat. The majority of the increased liver lipid can be accounted for by triglyceride accumulation. Increased liver lipid infiltration was found to be independent of the sex of the rat. Accompanying this increase was a decrease in serum triglycerides and cholesterol concentrations. Fatty infiltrations induced by arginine deficiency could be reversed by refeeding an arginine enriched diet. Adenine supplementation (0.30%) to the arginine deficient diet also completely prevented the induction of fatty livers. Adenine supplementation resulted in a dramatic increase in urinary orotic acid excretion in the arginine deficient rat. Guanine supplementation (0.5%) to an arginine deficient diet reduced but did not prevent the induction of fatty livers. The similarities of fatty livers induced by arginine deficiency and orotic acid feeding are discussed.
已知精氨酸缺乏会导致嘧啶生物合成发生显著改变以及尿乳清酸过度流失。已知喂食乳清酸会导致肝脂肪变性。这些研究表明，精氨酸缺乏还会导致大鼠肝脏脂质显著增加。肝脏脂质增加的大部分原因可归因于甘油三酯的积累。发现肝脏脂质浸润增加与大鼠性别无关。伴随这种增加的是血清甘油三酯和胆固醇浓度的降低。通过重新喂食富含精氨酸的饮食，可以逆转精氨酸缺乏引起的脂肪浸润。在精氨酸缺乏的饮食中添加腺嘌呤（0.30%）也完全预防了脂肪肝的形成。腺嘌呤的添加导致精氨酸缺乏大鼠尿乳清酸排泄显著增加。在精氨酸缺乏的饮食中添加鸟嘌呤（0.5%）可减少但不能预防脂肪肝的形成。本文讨论了精氨酸缺乏和喂食乳清酸所诱导的脂肪肝的相似之处。
