PROTECTION BY LACTATE OF CEREBRAL FUNCTION DURING HYPOGLYCEMIA
PROTECTION BY LACTATE OF CEREBRAL FUNCTION DURING HYPOGLYCEMIA
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DOI：
10.1016/s0140-6736(94)90876-1
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发表时间：
1994-01-01
期刊：
影响因子：
168.9
通讯作者：
AMIEL, SA
中科院分区：
文献类型：
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作者：
MARAN, A;CRANSTON, I;AMIEL, SA
伴有脑功能障碍的严重低血糖限制了胰岛素依赖型糖尿病患者的强化治疗，尽管有证据表明这种治疗降低了疾病慢性并发症的风险。我们研究了注入乳酸(一种潜在的非葡萄糖脑代谢燃料)对七名健康男性低血糖期间保护性、症状性神经体液反应和脑功能的影响。乳酸的升高(在生理范围内)显著减少儿茶酚胺、生长激素、皮质醇和对低血糖的症状反应，并降低了这些反应开始的葡萄糖水平。胰升糖素的反应没有受到影响。乳酸还与大脑功能恶化的血糖水平显著降低有关，这表明大脑功能在低血糖期间受到保护。反向调节缺陷类似于低血糖倾向的糖尿病患者。对低血糖的保护性反应(除高血糖素外)的启动可以通过替代代谢燃料的支持代谢来延迟。严重低血糖的大脑皮层功能障碍也延缓。我们的研究表明，低血糖时较高的大脑功能可以得到保护，这可能具有治疗潜力。
Severe hypoglycaemia with brain dysfunction limits intensified therapy in patients with insulin-dependent diabetes mellitus, despite evidence that such therapy reduces the risk of chronic complications of the disease. We have investigated the effect of infusing lactate (a potential non-glucose fuel for brain metabolism) on protective, symptomatic neurohumoral responses and on brain function during hypoglycaemia in seven healthy men.Elevation of lactate (within a physiological range) substantially diminished catecholamines, growth hormone, cortisol, and symptomatic responses to hypoglycaemia and lowered the glucose level at which these responses began. Glucagon responses were unaffected. Lactate was also associated with a significant lowering of the glucose level at which brain function deteriorated, suggesting that brain function was protected during the hypoglycaemia.The defect in counter-regulation is similar to that seen in hypoglycaemia-prone diabetic patients. Initiation of the protective responses to hypoglycaemia (except glucagon) can be delayed by supporting-metabolism with an alternative metabolic fuel. Cerebral cortical dysfunction of severe hypoglycaemia is also delayed. Our demonstration that higher brain function can be protected during hypoglycaemia may have therapeutic potential.