Diabetes-induced alterations of glucose metabolism in rat cerebral microvessels.

Diabetes-induced alterations of glucose metabolism in rat cerebral microvessels.
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糖尿病引起的大鼠脑微血管葡萄糖代谢的改变。

DOI:
10.1152/ajpendo.1984.247.4.e462
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发表时间:
1984
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Ruderman,NB
Ruderman,NB
中科院分区:
--
文献类型:
--
作者:
McCall,AL;Gould,JB;Ruderman,NB

文献摘要

被引文献

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在离体大鼠脑微血管中观察糖尿病对葡萄糖和乳酸代谢的影响。在链脲佐菌素诱导的糖尿病大鼠中,葡萄糖被微血管氧化为CO2减少54-83%,转化为乳酸减少21-61%。胰岛素治疗数天或饥饿48小时均可降低糖尿病大鼠的血糖水平,并使微血管葡萄糖代谢恢复正常。脑微血管主要由构成血脑屏障的毛细血管组成。使用脑摄取指数(BUI)技术直接评估体内血脑屏障的结果与微血管的结果非常相似。因此,糖尿病大鼠的己糖转运减少,并通过胰岛素治疗和饥饿恢复正常。糖尿病大鼠微血管中[1-14C]乳酸与葡萄糖一样氧化成CO2受到抑制。然而,与葡萄糖相反,乳酸在体内通过血脑屏障的转运并没有改变。这些发现表明糖尿病抑制了大鼠大脑微血管中的葡萄糖代谢,并下调了葡萄糖在血脑屏障中的转运。他们还认为,这两个过程都是由血糖浓度的慢性变化而不是胰岛素本身调节的。
The effect of diabetes on the metabolism of glucose and lactate was examined in isolated rat cerebral microvessels. In rats with diabetes induced with streptozotocin, glucose oxidation to CO2 by the microvessels was decreased by 54-83% and its conversion to lactate by 21-61%. Insulin therapy for several days or starvation for 48 h both lowered blood glucose levels in the diabetic rats and restored microvessel glucose metabolism to normal. Cerebral microvessels consist principally of the capillaries that constitute the blood-brain barrier. Direct assessment of the blood-brain barrier in vivo using the brain uptake index (BUI) technique revealed a close parallel to the findings in the microvessels. Thus, hexose transport was diminished in diabetic rats and restored to normal by both insulin therapy and starvation. The oxidation of [1-14C]lactate to CO2 like that of glucose was depressed in microvessels of diabetic rats. In contrast to glucose, however, the transport of lactate across the blood-brain barrier in vivo was not altered. These findings suggest that diabetes suppresses glucose metabolism in rat cerebral microvessels and downregulates glucose transport across the blood-brain barrier. They also suggest that both of these processes are regulated by chronic alterations in blood glucose concentration rather than by insulin per se.