McCall A L, Gould J B, Ruderman N B
Am J Physiol. 1984 Oct;247(4 Pt 1):E462-7. doi: 10.1152/ajpendo.1984.247.4.E462.
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.
在分离的大鼠脑微血管中研究了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,微血管将葡萄糖氧化为二氧化碳的能力降低了54%至83%,其转化为乳酸的能力降低了21%至61%。对糖尿病大鼠进行数天的胰岛素治疗或48小时的饥饿处理,均可降低其血糖水平,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)技术对体内血脑屏障进行的直接评估显示,其结果与微血管中的发现密切相关。因此,糖尿病大鼠的己糖转运减少,胰岛素治疗和饥饿均可使其恢复正常。糖尿病大鼠微血管中,[1-14C]乳酸氧化为二氧化碳的过程与葡萄糖类似,均受到抑制。然而,与葡萄糖不同的是,体内乳酸跨血脑屏障的转运未发生改变。这些发现表明,糖尿病会抑制大鼠脑微血管中的葡萄糖代谢,并下调葡萄糖跨血脑屏障的转运。它们还表明,这两个过程均受血糖浓度的长期变化调节,而非胰岛素本身。