UREMIA, ACIDOSIS & DIALYSIS ON PROTEIN METABOLISM: LONGITUDINAL LEUCINE KINETICS

尿毒症和透析被视为分解代谢过程，导致 慢性肾功能衰竭(CRF)患者的营养不良要理清 尿毒症、酸中毒和透析对蛋白质代谢的影响 慢性肾功能衰竭患者治疗前后亮氨酸流量的测定 维持性透析。通过测量全身亮氨酸流量 L[1-13C]亮氨酸预充持续输注治疗慢性肾功能衰竭9例 纵向；维修开始前两次，维修后一次 透析[D]。在透析前，测量一个亮氨酸流量，当 2名患者患有酸中毒[A]，另一名患者在酸中毒纠正后 用NaHCO3[NA]。5名正常受试者接受了单次亮氨酸试验 流量测量作为控制[N]。无论是患者还是正常人 受试者连续6天摄入恒定饮食，亮氨酸流量为 测量时间为第7天12小时。后吸收。慢性肾衰患者的饮食 患者在这三个时期是相同的。血浆L[1-13C] 用气相色谱/质谱法测定了亮氨酸和L的[1-13C]KIC 用同位素比值光谱分析了过期的13CO2。亮氨酸 动力学用标准方程计算。血浆中的二氧化碳 A期、NA期和D期分别为19、26和31 mmoL/L。全部动能 结果(摩尔/公斤/小时)表示为平均值(按A、NA、 D和N，以及与N有统计差异的CRF值为 已标识[*]。内源性蛋白质中亮氨酸的释放量 分解[Ra或Q]为101(12*，95(9*，113(22和117(6)亮氨酸 氧化[C]，不可逆地氧化成二氧化碳的亮氨酸的量，是 16.5(5.4、9.7(3.7*、12.3(3.0*及23.2(3.1亮氨酸蛋白 成立为[S]的人数为85(10，85(8,101)19及94(6)101的S CRF患者D期显著高于A期 和NA句号。这些数据表明，当酸中毒得到纠正时， 慢性肾衰患者通过减少氨基酸摄入来适应低蛋白质摄入量 氧化和蛋白质降解，并维持蛋白质合成在 正常水平。代谢性酸中毒损害血管紧张素转换酶的下调 氨基酸氧化。纵向维持性透析治疗 蛋白质流量恢复到正常水平，蛋白质合成增加。这个 一般认为尿毒症和透析是蛋白质分解代谢的，但不是 在这项工作的支持下。

Uremia and dialysis are viewed as catabolic processes resulting in malnutrition in chronic renal failure (CRF) patients. To sort out the effects of uremia, acidosis and dialysis on protein metabolism, we measured leucine flux in CRF patients before and after initiation of maintenance dialysis. Whole body leucine flux was measured by primed-constant infusion of L[1-13C]leucine in 9 CRF patients longitudinally; twice before and once after initiation of maintenance dialysis [D]. Before dialysis, one leucine flux was measured when the patients were acidotic [A], and the other, when acidosis was corrected with NaHCO3[NA]. Five normal subjects underwent one single leucine flux measurement to serve as control [N]. Both patients and normal subjects consumed a constant diet for 6 days and leucine flux was measured on the 7th day 12 hr. post-absorption. Diet for the CRF patients was identical during the three periods. Plasma L[1-13C] leucine and L[1-13C]KIC were measured by gas c hromatography/mass spectrometry and expired 13CO2 by isotope ratio spectrometry. Leucine kinetics were calculated using standard equations. Plasma CO2 were 19,26 and 31 mmol/L in A, NA and D periods, respectively. All kinetic results ((mol/kg/hr) are presented as means (SD in the order of A, NA, D and N, and CRF values that are statistically different from N are identified [*]. The amount of leucine release from endogenous protein breakdown [Ra or Q] were 101(12*, 95(9*, 113(22 and 117(6. Leucine oxidation [C], quantity of leucine irreversibly oxidized to CO2, were 16.5(5.4, 9.7(3.7*, 12.3(3.0* and 23.2(3.1. Leucine protein incorporation [S] were 85(10, 85(8, 101(19 and 94(6. The S of 101 in CRF patients at period D was statistically higher than those during A and NA periods. These data indicate that when acidosis was corrected, CRF patients adapted to lower protein intake by reducing amino acid oxidation and protein degradation, and maintained protein synthesis at normal level . Metabolic acidosis impaired the down regulation of amino acid oxidation. Maintenance dialysis treatment longitudinally restored protein flux to normal and increased protein synthesis. The general notion that uremia and dialysis are protein catabolic are not supported by this work.