Department of Surgery, Maastricht University Medical Center, Maastricht, The Netherlands.
Am J Clin Nutr. 2010 Apr;91(4):992-1001. doi: 10.3945/ajcn.2009.27812. Epub 2010 Feb 10.
Inadequate caloric intake increases the risk of sepsis-induced complications. Metabolic changes during sepsis indicate that the availability of the amino acid l-arginine decreases. Availability of arginine may further decrease during reduced caloric intake, which thereby limits the adaptive response of arginine-nitric oxide metabolism during sepsis.
We tested the hypothesis that reduced caloric intake during endotoxemia, as an experimental model for sepsis, further reduces arginine availability.
In a randomized trial, a 7-d reduced caloric intake feed regimen (RE; n = 9) was compared with a normal control feed regimen (CE; n = 9), before 24 h of endotoxemia, as a model for sepsis. Whole-body arginine-nitric oxide metabolism and protein metabolism were measured by using a stable-isotope infusion of [(15)N(2)]arginine, [(13)C-(2)H(2)]citrulline, [(2)H(5)]phenylalanine, and [(2)H(2)]tyrosine. Plasma pyruvate and lactate concentrations were determined by fully automated HPLC.
Pre-endotoxin arginine appearance was significantly lower in the RE group than in the CE group (P = 0.002). During endotoxemia, arginine appearance increased in the CE animals but not in the RE animals (P = 0.04). In addition, nitric oxide production was significantly lower in the RE animals (P < 0.0001). Protein synthesis was significantly lower at the start of endotoxin infusion (P < 0.05) and remained lower during endotoxemia in the RE group than in the CE group (P < 0.001). The lactate:pyruvate ratio was not higher in the RE group than in the CE group before endotoxemia but increased significantly during endotoxemia in the RE group (P = 0.04).
A well-nourished condition before prolonged endotoxemia results in a better ability to adapt to endotoxin-induced metabolic deterioration of arginine-nitric oxide metabolism than does reduced caloric intake before endotoxemia.
热量摄入不足会增加脓毒症引起的并发症的风险。脓毒症期间的代谢变化表明,氨基酸 l-精氨酸的可用性降低。在热量摄入减少的情况下,精氨酸的可用性可能会进一步降低,从而限制了脓毒症期间精氨酸-一氧化氮代谢的适应性反应。
我们检验了这样一个假设,即在脓毒症的实验模型——内毒素血症期间,减少热量摄入会进一步降低精氨酸的可用性。
在一项随机试验中,在 24 小时内毒素血症前,将 7 天的低热量摄入喂养方案(RE;n=9)与正常对照喂养方案(CE;n=9)进行比较,以模拟脓毒症。通过稳定同位素输注[(15)N2]精氨酸、[(13)C-(2)H2]瓜氨酸、[(2)H5]苯丙氨酸和[(2)H2]酪氨酸来测量全身精氨酸-一氧化氮代谢和蛋白质代谢。通过全自动 HPLC 测定血浆丙酮酸和乳酸浓度。
在 RE 组,预内毒素精氨酸出现率明显低于 CE 组(P=0.002)。在内毒素血症期间,CE 组的精氨酸出现率增加,而 RE 组没有增加(P=0.04)。此外,RE 组的一氧化氮生成量明显较低(P<0.0001)。在开始输注内毒素时,蛋白质合成明显较低(P<0.05),并且在 RE 组,蛋白质合成在整个内毒素血症期间均低于 CE 组(P<0.001)。在 RE 组,与 CE 组相比,在预内毒素血症时,乳酸:丙酮酸比值并不更高,但在 RE 组,该比值在内毒素血症期间显著增加(P=0.04)。
在内毒素血症前营养良好的条件会导致更好地适应内毒素引起的精氨酸-一氧化氮代谢代谢恶化,而在内毒素血症前减少热量摄入则不会。