Jahoor Farook, Badaloo Asha, Reid Marvin, Forrester Terrence
US Department of Agriculture Agricultural Research Service, Children's Nutrition Research Center, Houston, TX 77030-2600, USA.
Am J Clin Nutr. 2005 Oct;82(4):792-800. doi: 10.1093/ajcn/82.4.792.
Pathogenic factors that cause a child to develop the edematous instead of the nonedematous form of severe childhood undernutrition (SCU) during food deprivation are not clear. It was hypothesized that, in edematous but not nonedematous SCU, impaired protein breakdown leading to inadequate amino acids for maintenance of important organ systems was a factor.
We measured protein kinetics in children with edematous and nonedematous SCU.
Endogenous leucine flux, an index of whole-body protein breakdown rate, was determined in 4 groups of children with edematous or nonedematous SCU in the malnourished and recovered states. Two groups were studied in the postabsorptive state, and 2 groups were studied in the fed state.
In the postabsorptive state, leucine flux was slower (P < 0.01) in the edematous group than in the nonedematous group in the malnourished state, but in the recovered state, it was faster (P < 0.05) in the children who previously had edematous SCU. When compared with the malnourished state value, leucine flux at recovery doubled in the group that previously had edematous SCU, but it did not change in the other group. In the fed state, leucine flux was slower (P < 0.01) in the edematous group than in the nonedematous group in the malnourished state but not in the recovered state. In the recovered state, enteral leucine extraction by splanchnic tissues trended higher in the group that previously had edematous SCU than in the nonedematous group.
These findings indicate different protein breakdown responses to food deprivation between children with edematous and nonedematous SCU and inherent differences in protein metabolism when they have recovered.
在食物匮乏期间,导致儿童出现重度儿童营养不良(SCU)水肿型而非非水肿型的致病因素尚不清楚。据推测,在水肿型而非非水肿型的SCU中,蛋白质分解受损导致维持重要器官系统所需的氨基酸不足是一个因素。
我们测量了水肿型和非水肿型SCU患儿的蛋白质动力学。
在4组处于营养不良和康复状态的水肿型或非水肿型SCU患儿中,测定了内源性亮氨酸通量,这是全身蛋白质分解率的一个指标。2组在空腹状态下进行研究,2组在进食状态下进行研究。
在空腹状态下,营养不良状态时水肿组的亮氨酸通量比非水肿组慢(P<0.01),但在康复状态下,先前患有水肿型SCU的儿童亮氨酸通量更快(P<0.05)。与营养不良状态值相比,先前患有水肿型SCU的组在康复时亮氨酸通量增加了一倍,但另一组没有变化。在进食状态下,营养不良状态时水肿组的亮氨酸通量比非水肿组慢(P<0.01),但在康复状态下并非如此。在康复状态下,先前患有水肿型SCU的组内脏组织对肠内亮氨酸的提取趋势高于非水肿组。
这些发现表明,水肿型和非水肿型SCU患儿对食物匮乏的蛋白质分解反应不同,且康复时蛋白质代谢存在内在差异。