Aperia A, Broberger O, Larsson A, Snellman K
Scand J Clin Lab Invest. 1979 Jun;39(4):329-36. doi: 10.3109/00365517909106116.
Activities of renal urea enzymes were studied in normally fed (21% dietary protein) rats and rats deprived of protein (6% dietary protein) for 3 weeks. Protein deprivation resulted in growth retardation and defective urine concentrating ability. Compared to rats on an optimal diet containing 21% of protein, the protein starved animals had decreased concentrations of protein and urea in serum, reduced urinary excretion of urea and decreased levels of all five urea cycle enzyme activities in the liver. In the kidney, however, protein malnutrition resulted in a significant increase in arginase specific activity from 11.5 +/- 1.1 to 16.3 +/- 1.5 (M +/- SD) whereas the other urea cycle enzymes remained unchanged. It is postulated that this increase in renal arginase might be an early compensatory mechanism to preserve a net synthesis of urea in a situation involving arginine deficiency, thereby preserving an intact hypertonic gradient in the renal medulla.
研究了正常喂食(饮食中蛋白质含量为21%)的大鼠和蛋白质缺乏(饮食中蛋白质含量为6%)3周的大鼠肾脏尿素酶的活性。蛋白质缺乏导致生长迟缓以及尿液浓缩能力缺陷。与食用含21%蛋白质的最佳饮食的大鼠相比,蛋白质饥饿的动物血清中蛋白质和尿素浓度降低,尿素尿排泄减少,肝脏中所有五种尿素循环酶活性水平降低。然而,在肾脏中,蛋白质营养不良导致精氨酸酶比活性从11.5±1.1显著增加至16.3±1.5(平均值±标准差),而其他尿素循环酶保持不变。据推测,肾脏中精氨酸酶的这种增加可能是一种早期代偿机制,以便在精氨酸缺乏的情况下维持尿素的净合成,从而维持肾髓质完整的高渗梯度。