EFFECTS OF ETHANOL ON GLUCOSE TRANSPORTER EXPRESSION

发育中的大脑对乙醇的毒性作用非常敏感，但这些作用的机制还不清楚。 有人提出，暴露的大脑发育乙醇的结果在特定的葡萄糖转运蛋白亚型GLUT 1和GLUT 3的调节。 也有人提出，在葡萄糖转运蛋白基因表达的改变可能会受到调节，在区域和/或细胞类型的特定方式在转录或转录后水平。 由葡萄糖转运蛋白水平变化引起的葡萄糖转运变化可能对未成熟脑细胞中重要的能量和合成途径以及自由基保护产生负面影响。 提出了研究，检查这些变化的基因表达使用体内模型描绘区域和细胞类型的差异，并使用神经元培养物，以进一步表征的效果和可能的潜在机制，包括对转录，信息稳定性的影响，并改变核糖核蛋白的影响信息的稳定性和翻译。 这项研究的长期前景是，彻底了解产前酒精暴露和胎儿酒精综合征的表现之间的联系，将导致开发有效的治疗策略，以尽量减少或消除损害。

The developing brain is extremely sensitive to the toxic effects of ethanol, but the mechanisms underlying these effects are not well understood. It is proposed that exposure of the developing brain to ethanol results in the specific regulation of the glucose transporter isoforms GLUT1 and GLUT3. It is also proposed that alterations in glucose transporter gene expression may be regulated in a regional and or cell-type specific manner at transcriptional or posttranscriptional levels. Changes in glucose transport, resulting from changes in the levels of glucose transporter proteins, may have a negative impact on important energy and synthetic pathways, as well as protection from free radicals, in immature brain cells. Studies are proposed which examine these changes in gene expression using an in vivo model to delineate regional and cell type differences and using neuronal cultures to further characterize the effect and possible underlying mechanisms, including effects on transcription, message stability, and altered ribonucleoproteins which influence message stability and translation. The long term prospects of this study are that a thorough understanding of the connection between prenatal alcohol exposure and the manifestations of Fetal Alcohol Syndrome will lead to development of effective treatment strategies to minimize or eliminate impairments.