Brain glucose transporter (Glut3) haploinsufficiency does not impair mouse brain glucose uptake.
Brain glucose transporter (Glut3) haploinsufficiency does not impair mouse brain glucose uptake.
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DOI：
10.1016/j.brainres.2011.02.014
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发表时间：
2011-04-12
期刊：
影响因子：
2.9
通讯作者：
Wall J
中科院分区：
文献类型：
--
作者：
Stuart CA;Ross IR;Howell ME;McCurry MP;Wood TG;Ceci JD;Kennel SJ;Wall J
小鼠大脑表达三种主要的葡萄糖转运蛋白。Glut 1是一种内皮标志物，是血脑屏障的主要葡萄糖转运蛋白。Glut 3和Glut 6在神经胶质细胞和神经细胞中表达。已经开发了具有Glut 3无效等位基因的小鼠品系。Glut 3 −/−基因型在交配后7天内是宫内致死的，但杂合子（Glut 3 +/−）同窝仔存活，表现出出生后体重迅速增加，但没有癫痫发作或其他行为异常。在12周龄时，Glut 3 +/−小鼠的尾静脉注射3 H-2-脱氧葡萄糖的脑摄取与Glut 3 +/+同窝小鼠没有差异，尽管大脑中Glut 3蛋白表达减少了50%。注射的18 F-2-氟-2-脱氧葡萄糖的脑摄取在总量、时程或Glut 3 +/−小鼠的脑成像方面与Glut 3 +/−同窝小鼠相似。通过免疫印迹评估的Glut 1和Glut 6蛋白表达不受Glut 3 +/−小鼠中Glut 3表达减少的影响。我们的结论是，50%的Glut 3减少是不限制葡萄糖的摄取到小鼠大脑中，因为Glut 3单倍不足不损害大脑葡萄糖的摄取或利用。
Mouse brain expresses three principle glucose transporters. Glut1 is an endothelial marker and is the principal glucose transporter of the blood-brain barrier. Glut3 and Glut6 are expressed in glial cells and neural cells. A mouse line with a null allele for Glut3 has been developed. The Glut3−/− genotype is intrauterine lethal by seven days post-coitis, but the heterozygous (Glut3+/−) littermate survives, exhibiting rapid post-natal weight gain, but no seizures or other behavioral aberrations. At twelve weeks of age, brain uptake of tail vein-injected 3H-2-deoxy glucose in Glut3+/− mice was not different from Glut3+/+ littermates, despite 50% less Glut3 protein expression in the brain. The brain uptake of injected 18F-2-fluoro-2-deoxy glucose was similarly not different from Glut3+/− littermates in the total amount, time course, or brain imaging in the Glut3+/− mice. Glut1 and Glut6 protein expressions evaluated by immunoblots were not affected by the diminished Glut3 expression in the Glut3+/− mice. We conclude that a 50% decrease in Glut3 is not limiting for the uptake of glucose into the mouse brain, since Glut3 haploinsufficiency does not impair brain glucose uptake or utilization.
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影响因子：
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