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链脲佐菌素诱导的糖尿病中的脑能量代谢

Brain energy metabolism in streptozotocin-diabetes.

作者信息

Mans A M, DeJoseph M R, Davis D W, Hawkins R A

机构信息

Department of Anesthesia, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey 17033.

出版信息

Biochem J. 1988 Jan 1;249(1):57-62. doi: 10.1042/bj2490057.

Abstract

Regional brain glucose use was measured in rats with streptozotocin-induced diabetes (65 mg/kg intravenously) of 1 or 4 weeks duration, by using [6-14C]glucose and quantitative autoradiography. The concentrations of several metabolites were measured in plasma and brain. Results were compared with those from normal untreated rats. Glucose concentrations were increased in both plasma and brain, to similar degrees in both diabetic groups. Plasma ketone-body concentrations were 0.25, 1.0, and 3.15 mumol/ml in the control, 1-week and 4-week groups respectively (sum of acetoacetate and 3-hydroxybutyrate). Glucose use was increased throughout the brain (differences were statistically significant in 55 of 59 brain areas) after 1 week of diabetes, with an increase of 25% for the brain as a whole. In contrast, normal rates were found throughout the brain after 4 weeks of diabetes. None of the brain areas was affected significantly differently from the others, in either diabetic group. There was no significant loss of 14C as lactate or pyruvate during the experimental period, nor was there any indication of net production of lactate in any of the groups. Other methodological considerations that could have affected the results obtained in the diabetic rats were likewise ruled out. Because the ketone bodies are expected to supplement glucose as a metabolic fuel for the brain, our results indicate that brain energy consumption is increased during streptozotocin-diabetes.

摘要

采用[6-14C]葡萄糖和定量放射自显影技术,对链脲佐菌素诱导的糖尿病大鼠(静脉注射65mg/kg,病程1周或4周)的脑区葡萄糖利用情况进行了测定。同时测定了血浆和脑中几种代谢物的浓度。将结果与正常未处理大鼠的结果进行比较。血浆和脑中的葡萄糖浓度均升高,两个糖尿病组的升高程度相似。对照组、1周组和4周组的血浆酮体浓度分别为0.25、1.0和3.15μmol/ml(乙酰乙酸和3-羟基丁酸之和)。糖尿病1周后,全脑葡萄糖利用增加(59个脑区中有55个脑区差异具有统计学意义),全脑葡萄糖利用增加25%。相比之下,糖尿病4周后全脑葡萄糖利用率恢复正常。在两个糖尿病组中,各脑区受影响程度无显著差异。实验期间,未发现14C以乳酸或丙酮酸形式显著丢失,各实验组也均未显示有乳酸净生成的迹象。同样排除了其他可能影响糖尿病大鼠实验结果的方法学因素。由于酮体有望作为脑代谢燃料补充葡萄糖,我们的结果表明,链脲佐菌素诱导的糖尿病期间脑能量消耗增加。

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