Gore Dennis C, Wolfe Robert R
Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77555-1172, USA.
JPEN J Parenter Enteral Nutr. 2003 Sep-Oct;27(5):307-14. doi: 10.1177/0148607103027005307.
Alanine and glutamine are released from muscle in response to critical illness. Subsequent depletion of glutamine from muscle is proposed as a principal factor in the limitation of muscle protein synthesis in severely ill patients. The objective of this study was to assess the peripheral metabolic response to enteral supplementation of alanine, glutamine, and valine in critically ill patients.
Isotopic tracers of alanine, glutamine, and phenylalanine were given IV to 6 critically ill patients and 6 healthy volunteers. Blood sampling from the femoral artery and vein along with muscle biopsies provided assessment of leg (ie, muscle) kinetics. Measurements were obtained during enteral nutrition alone and then with combined alanine (11.25 g), glutamine (7.5 g) and valine (11.25 g) supplementation for 3 hours.
Compared with healthy volunteers, critically ill patients had significantly reduced concentrations of alanine and glutamine in arterial plasma (p < .05), which increased significantly with amino acid supplementation. Muscle glutamine concentrations were significantly less in the patients and were not significantly affected by supplementation. Alanine and glutamine transport into and out of muscle and the rates of alanine and glutamine incorporation into and production from muscle were not affected by supplementation. Phenylalanine kinetics, as a marker of muscle protein metabolism, were not significantly altered by alanine, glutamine, and valine intake.
These results demonstrate that alanine, glutamine, and valine administration fails to significantly affect muscle glutamine availability or muscle protein metabolism. These findings suggest that accelerated muscle catabolism in critically ill patients is not in response to any deficiency in alanine or glutamine availability.
丙氨酸和谷氨酰胺会在危重病期间从肌肉中释放出来。随后肌肉中谷氨酰胺的消耗被认为是重症患者肌肉蛋白质合成受限的主要因素。本研究的目的是评估危重病患者肠内补充丙氨酸、谷氨酰胺和缬氨酸后的外周代谢反应。
对6例危重病患者和6名健康志愿者静脉注射丙氨酸、谷氨酰胺和苯丙氨酸的同位素示踪剂。通过股动脉和静脉采血以及肌肉活检来评估腿部(即肌肉)动力学。在仅进行肠内营养期间以及随后联合补充丙氨酸(11.25克)、谷氨酰胺(7.5克)和缬氨酸(11.25克)3小时后进行测量。
与健康志愿者相比,危重病患者动脉血浆中的丙氨酸和谷氨酰胺浓度显著降低(p < 0.05),补充氨基酸后显著升高。患者的肌肉谷氨酰胺浓度显著较低,且补充对其无显著影响。丙氨酸和谷氨酰胺进出肌肉的转运以及丙氨酸和谷氨酰胺在肌肉中的掺入和生成速率不受补充的影响。作为肌肉蛋白质代谢标志物的苯丙氨酸动力学未因丙氨酸、谷氨酰胺和缬氨酸的摄入而显著改变。
这些结果表明,给予丙氨酸、谷氨酰胺和缬氨酸未能显著影响肌肉谷氨酰胺的可利用性或肌肉蛋白质代谢。这些发现表明,危重病患者肌肉分解代谢加速并非对丙氨酸或谷氨酰胺可利用性的任何缺乏做出反应。