Chronic insulin hypoglycemia induces GLUT-3 protein in rat brain neurons.
Chronic insulin hypoglycemia induces GLUT-3 protein in rat brain neurons.
复制标题
慢性胰岛素低血糖会在大鼠脑神经元中诱导 GLUT-3 蛋白。
DOI：
10.1152/ajpendo.1997.272.4.e716
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
McCall,AL
中科院分区：
文献类型：
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作者：
Uehara,Y;Nipper,V;McCall,AL
血糖接近正常降低了糖尿病慢性并发症的风险，但增加了严重低血糖的风险。低血糖可以损害大脑中的神经元功能，并降低对后续低血糖发作的意识，但对于神经元如何适应低血糖知之甚少。这项研究测试了一种假设，即大脑葡萄糖运输蛋白的异构体特异性变化是对慢性低血糖的反应。为了研究这一点，各组大鼠在1700℃每天注射大约25U/kg的超低密度胰岛素，持续8天以维持低血糖。制备GLUT-1和GLUT-3的无血管和微血管膜组分，用异构体特异性抗血清进行免疫印迹分析。胰岛素治疗使血糖水平在第8天从载体注射对照组的4.0/-0.1降至1.7/-0.1mmo1/L(P<；0.001)，并增加了Glut-3蛋白的表达(对照组的2.0%；P<；0.0 5)。微血管GLUT-1(55 KDa)有不同程度的增加趋势(195.6%，P=0.08)，而非血管GLUT-1(45 KDa)无明显变化。我们认为神经细胞葡萄糖转运蛋白(GLUT-3)的表达适应慢性低血糖。这种适应可能会减少神经元的能量代谢，但可能会抑制葡萄糖剥夺的神经元信号。
Near-normalization of glycemia reduces the risks of chronic diabetic complications but increases the risk of serious hypoglycemia. Hypoglycemia can impair neuronal function in the brain and diminish awareness of subsequent hypoglycemic episodes, yet little is known about how neurons adapt to hypoglycemia. This study tests the hypothesis that isoform-specific alterations in brain glucose transport proteins occur in response to chronic hypoglycemia. To study this, groups of rats were injected with approximately 25 U/kg ultralente insulin daily at 1700 for 8 days to maintain hypoglycemia. Vascular-free and microvessel membrane fractions from brain were prepared for immunoblot analysis of GLUT-1 and GLUT-3 by use of isoform-specific antisera. Insulin treatment reduced blood glucose levels from 4.0 +/- 0.1 (vehicle-injected controls) to 1.7 +/- 0.1 mmol/l on day 8 (P < 0.001) and increased GLUT-3 protein expression (175.6% of control; P < 0.05). Microvascular GLUT-1 (55 kDa) tended to increase (195.6% of controls; P = 0.08) variably, whereas nonvascular GLUT-1 (45 kDa) was unchanged. We conclude that neuronal glucose transport protein (GLUT-3) expression adapts to chronic hypoglycemia. This adaptation may spare neuronal energy metabolism but could dampen neuronal signaling of glucose deprivation.