Glucose and glutamine metabolism in the small intestine of septic rats.
Glucose and glutamine metabolism in the small intestine of septic rats.
复制标题
脓毒症大鼠小肠中的葡萄糖和谷氨酰胺代谢。
DOI：
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发表时间：
1990
期刊：
影响因子：
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通讯作者：
E. Newsholme
中科院分区：
文献类型：
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作者：
M. Ardawi;Y. Jamal;A. Ashy;H. Nasr;E. Newsholme
研究了通过盲肠结扎和穿刺技术造成脓毒症的大鼠肠道中葡萄糖和谷氨酰胺的代谢。脓毒症导致负氮平衡，导致血液丙酮酸、乳酸、丙氨酸和谷氨酰胺浓度升高，而3-羟基丁酸和乙酰乙酸浓度降低。脓毒症大鼠的血浆胰岛素和胰高血糖素浓度分别增加了 2.2 倍和 3.2 倍。与假手术动物相比，脓毒症大鼠的门静脉引流内脏血流量增加，并且谷氨酰胺的利用率以及乳酸、谷氨酸和氨的产生率降低。与从相应对照中分离的细胞相比，从脓毒症大鼠中分离的肠细胞显示出葡萄糖和谷氨酰胺利用率降低。脓毒症大鼠肠粘膜刮片中己糖激酶、6-磷酸果糖激酶、丙酮酸激酶和谷氨酰胺酶的最大活性降低。结论是，中度脓毒症会降低小肠上皮细胞对葡萄糖和谷氨酰胺的利用率（体内和体外）。这可能是由于这些细胞中葡萄糖和谷氨酰胺代谢途径中关键酶的最大活性发生变化所致，这是一种代谢适应，以节省葡萄糖和谷氨酰胺供其他组织使用。
The intestinal metabolism of glucose and glutamine was studied in rats made septic by cecal ligation and puncture technique. Sepsis resulted in negative nitrogen balance and produced increases in the concentrations of blood pyruvate, lactate, alanine, and glutamine, and decreases in those of 3-hydroxybutyrate and acetoacetate. Both plasma insulin and glucagon concentrations were increased by 2.2- and 3.2-fold in septic rats, respectively. Portal-drained visceral blood flow increased in septic rats, and was accompanied by a decrease in the rates of utilization of glutamine and production of lactate, glutamate, and ammonia compared with those rates in sham-operated animals. Enterocytes isolated from septic rats showed decreased rates of glucose and glutamine utilization compared with cells isolated from corresponding controls. The maximal activities of hexokinase, 6-phosphofructokinase, pyruvate kinase, and glutaminase were decreased in intestinal mucosal scrapings of septic rats. It is concluded that a moderate form of sepsis decreases the rates of glucose and glutamine utilization (both in vivo and in vitro) by the epithelial cells of the small intestine. This may be caused by changes in the maximal activities of key enzymes in the pathways of glucose and glutamine metabolism in these cells as a metabolic adaptation to spare glucose and glutamine for use by other tissues.