Ardawi M S, Majzoub M F, Kateilah S M, Newsholme E A
Department of Clinical Biochemistry, College of Medicine and Allied Sciences, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
J Lab Clin Med. 1991 Jul;118(1):26-32.
The activity of phosphate-dependent glutaminase and glutamine metabolism by tissues known markedly to utilize or synthesize glutamine (or both) were studied in rats made septic by cecal ligation and puncture technique and compared with the same measures in rats that underwent sham operation (laparotomy). Blood glucose level was not markedly different in septic rats, but lactate, pyruvate, alanine, and glutamine levels were markedly increased. Conversely, blood ketone body concentrations were significantly decreased in septic rats. Both plasma insulin and glucagon levels were markedly elevated in response to sepsis. The maximal activity of phosphate-dependent glutaminase was decreased in the small intestine, increased in the kidney and mesenteric lymph nodes, and unchanged in the liver of septic rats. Arteriovenous concentration difference measurements across the gut showed a decrease in the net glutamine removed from the circulation in septic rats. Arteriovenous concentration difference measurements for glutamine showed that both renal uptake and skeletal muscle release of the amino acid were increased in response to sepsis, whereas measurements across the hepatic bed showed a net uptake of glutamine in septic rats. Enterocytes isolated from septic rats exhibited a decreased rate of utilization of glutamine and production of glutamate, alanine, and ammonia, whereas lymphocytes isolated from septic rats showed an enhanced rate of utilization of glutamine and production of glutamate, aspartate, and ammonia. It is concluded that, during sepsis, glutamine uptake and metabolism are enhanced in renal and lymphoid tissue but decreased in that of the small intestine, with increased rates of release by skeletal muscle; however, the liver appears to utilize glutamine in septic rats.
采用盲肠结扎穿刺技术使大鼠发生脓毒症,研究了已知显著利用或合成谷氨酰胺(或两者皆有)的组织中磷酸依赖性谷氨酰胺酶的活性及谷氨酰胺代谢情况,并与接受假手术(剖腹术)的大鼠的相同指标进行比较。脓毒症大鼠的血糖水平无明显差异,但乳酸、丙酮酸、丙氨酸和谷氨酰胺水平显著升高。相反,脓毒症大鼠的血酮体浓度显著降低。脓毒症时,血浆胰岛素和胰高血糖素水平均显著升高。脓毒症大鼠小肠中磷酸依赖性谷氨酰胺酶的最大活性降低,肾脏和肠系膜淋巴结中该酶活性升高,肝脏中该酶活性无变化。对肠道进行的动静脉浓度差测量显示,脓毒症大鼠从循环中清除的谷氨酰胺净量减少。谷氨酰胺的动静脉浓度差测量表明,脓毒症时该氨基酸的肾脏摄取和骨骼肌释放均增加,而对肝脏床进行的测量显示脓毒症大鼠肝脏对谷氨酰胺有净摄取。从脓毒症大鼠分离的肠上皮细胞谷氨酰胺利用速率及谷氨酸、丙氨酸和氨的生成速率降低,而从脓毒症大鼠分离的淋巴细胞谷氨酰胺利用速率及谷氨酸、天冬氨酸和氨的生成速率增强。结论是,脓毒症期间,肾脏和淋巴组织中谷氨酰胺的摄取和代谢增强,但小肠中谷氨酰胺的摄取和代谢降低,骨骼肌释放谷氨酰胺的速率增加;然而,脓毒症大鼠的肝脏似乎利用谷氨酰胺。