Ban Kechen, Kozar Rosemary A
Department of Surgery, University of Texas Health Science Center of Houston, 6431 Fannin, MSB 4.284, Houston, TX 77030, USA.
J Leukoc Biol. 2008 Sep;84(3):595-9. doi: 10.1189/jlb.1107764. Epub 2008 Apr 7.
Early enteral nutrition supplemented with glutamine, arginine, omega-3 fatty acids, and nucleotides has been shown to decrease infection complications in critically injured patients. Concern has been raised, however, that under conditions of hyperinflammation, these diets may be injurious through the induction of inducible NO synthase by enteral arginine. In a rodent model of gut ischemia/reperfusion, inflammation and injury are intensified by enteral arginine and abrogated by glutamine. These findings correlate with the degree of metabolic stress imposed upon the gut by hypoperfusion. Glutamine is metabolized by the gut and therefore, can contribute back energy in the form of ATP, whereas arginine is a nonmetabolizable nutrient, using but not contributing energy. Recent data suggest that one of the molecular mechanisms responsible for the gut-protective effects of enteral glutamine is the activation of peroxisome proliferator-activated receptor gamma. This anti-inflammatory transcription factor belongs to the family of nuclear receptors, plays a key role in adipocyte development and glucose homeostasis, and has been recognized as an endogenous regulator of intestinal inflammation. Preliminary clinical studies support the use of enteral glutamine in patients with gut hypoperfusion.
已证明，补充谷氨酰胺、精氨酸、ω-3脂肪酸和核苷酸的早期肠内营养可降低重症受伤患者的感染并发症。然而，有人担心，在炎症反应过度的情况下，这些饮食可能会通过肠内精氨酸诱导诱导型一氧化氮合酶而造成损害。在肠道缺血/再灌注的啮齿动物模型中，肠内精氨酸会加剧炎症和损伤，而谷氨酰胺可消除这种情况。这些发现与低灌注对肠道造成的代谢应激程度相关。谷氨酰胺可被肠道代谢，因此可以以ATP的形式提供能量，而精氨酸是一种不可代谢的营养素，只消耗能量而不提供能量。最近的数据表明，肠内谷氨酰胺肠道保护作用的分子机制之一是过氧化物酶体增殖物激活受体γ的激活。这种抗炎转录因子属于核受体家族，在脂肪细胞发育和葡萄糖稳态中起关键作用，并且已被认为是肠道炎症的内源性调节剂。初步临床研究支持在肠道低灌注患者中使用肠内谷氨酰胺。
