Castillo L, Chapman T E, Sanchez M, Yu Y M, Burke J F, Ajami A M, Vogt J, Young V R
Laboratory of Human Nutrition, School of Science, Massachusetts Institute of Technology, Cambridge 02139.
Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7749-53. doi: 10.1073/pnas.90.16.7749.
The fluxes of arginine and citrulline through plasma and the rate of conversion of labeled citrulline to arginine were estimated in two pilot studies (with a total of six adult subjects) and in a dietary study with five healthy young men. These latter subjects received an L-amino acid-based diet that was arginine-rich or arginine-free each for 6 days prior to conduct, on day 7, of an 8-hr (first 3 hr, fast; final 5 hr, fed) primed continuous intravenous infusion protocol using L-[guanidino-13C]arginine, L-[5,5-2H2]citrulline, and L-[5,5,5-2H3]leucine, as tracers. A pilot study indicated that citrulline flux was about 20% higher (P < 0.05) when determined with [ureido-13C]citrulline compared with [2H2]citrulline, indicating recycling of the latter tracer. Mean citrulline fluxes were about 8-11 mumol.kg-1.hr-1 for the various metabolic/diet groups and did not differ significantly between fast and fed states or arginine-rich and arginine-free periods. Arginine fluxes (mean +/- SD) were 60.2 +/- 5.4 and 73.3 +/- 13.9 mumol.kg-1.hr-1 for fast and fed states during the arginine-rich period, respectively, and were significantly lowered (P < 0.05), by 20-40%, during the arginine-free period, especially for the fed state, where this was due largely to reduced entry of dietary arginine into plasma. The conversion of plasma citrulline to arginine approximated 5.5 mumol.kg-1.hr-1 for the various groups and also was unaffected by arginine intake. Thus, endogenous arginine synthesis is not markedly responsive to acute alterations in arginine intake in healthy adults. We propose that arginine homeostasis is achieved largely via modulating arginine intake and/or the net rate of arginine degradation.
在两项初步研究（共六名成年受试者）以及一项针对五名健康年轻男性的饮食研究中，对精氨酸和瓜氨酸通过血浆的通量以及标记瓜氨酸向精氨酸的转化速率进行了估算。后一组受试者在进行为期8小时（前3小时禁食；最后5小时进食）的静脉持续输注试验前6天，分别接受富含精氨酸或不含精氨酸的基于L - 氨基酸的饮食。该试验使用L - [胍基 - 13C]精氨酸、L - [5,5 - 2H2]瓜氨酸和L - [5,5,5 - 2H3]亮氨酸作为示踪剂。一项初步研究表明，与[2H2]瓜氨酸相比，用[脲基 - 13C]瓜氨酸测定时瓜氨酸通量高约20%（P < 0.05），这表明后一种示踪剂存在循环利用。不同代谢/饮食组的平均瓜氨酸通量约为8 - 11 μmol·kg-1·hr-1，在禁食和进食状态或富含精氨酸和不含精氨酸的时期之间无显著差异。在富含精氨酸时期，禁食和进食状态下的精氨酸通量（平均值±标准差）分别为60.2±5.4和73.3±13.9 μmol·kg-1·hr-1，在不含精氨酸时期显著降低（P < 0.05），降低了20 - 40%，尤其是在进食状态下，这主要是由于饮食中精氨酸进入血浆的量减少。不同组血浆瓜氨酸向精氨酸的转化约为5.5 μmol·kg-1·hr-1，且不受精氨酸摄入量的影响。因此，健康成年人内源性精氨酸合成对精氨酸摄入量的急性变化无明显反应。我们认为，精氨酸稳态主要通过调节精氨酸摄入量和/或精氨酸降解的净速率来实现。
