Funari Vincent A, Crandall James E, Tolan Dean R
Department of Biology, Boston University, Boston, Massachusetts 02215, USA.
Cerebellum. 2007;6(2):130-40. doi: 10.1080/14734220601064759.
Under normal physiological conditions, the brain utilizes only a small number of carbon sources for energy. Recently, there is growing molecular and biochemical evidence that other carbon sources, including fructose, may play a role in neuro-energetics. Fructose is the number one commercial sweetener in Western civilization with large amounts of fructose being toxic, yet fructose metabolism remains relatively poorly characterized. Fructose is purportedly metabolized via either of two pathways, the fructose-1-phosphate pathway and/or the fructose-6-phosphate pathway. Many early metabolic studies could not clearly discriminate which of these two pathways predominates, nor could they distinguish which cell types in various tissues are capable of fructose metabolism. In addition, the lack of good physiological models, the diet-induced changes in gene expression in many tissues, the involvement of multiple genes in multiple pathways involved in fructose metabolism, and the lack of characterization of some genes involved in fructose metabolism have complicated our understanding of the physiological role of fructose in neuro-energetics. A recent neuro-metabolism study of the cerebellum demonstrated fructose metabolism and co-expression of the genes specific for the fructose 1-phosphate pathway, GLUT5 (glut5) and ketohexokinase (khk), in Purkinje cells suggesting this as an active pathway in specific neurons? Meanwhile, concern over the rapid increase in dietary fructose, particularly among children, has increased awareness about how fructose is metabolized in vivo and what effects a high fructose diet might have. In this regard, establishment of cellular and molecular studies and physiological characterization of the important and/or deleterious roles fructose plays in the brain is critical. This review will discuss the status of fructose metabolism in the brain with special reference to the cerebellum and the physiological roles of the different pathways.
在正常生理条件下,大脑仅利用少量碳源来获取能量。最近,越来越多的分子和生化证据表明,包括果糖在内的其他碳源可能在神经能量代谢中发挥作用。果糖是西方文明中头号商业甜味剂,大量果糖具有毒性,然而果糖代谢的特征仍相对不明确。据称,果糖通过两条途径之一进行代谢,即1-磷酸果糖途径和/或6-磷酸果糖途径。许多早期的代谢研究无法清楚地区分这两条途径中哪一条占主导地位,也无法区分不同组织中的哪些细胞类型能够进行果糖代谢。此外,缺乏良好的生理模型、饮食引起的许多组织中基因表达的变化、果糖代谢涉及的多个途径中多个基因的参与,以及一些参与果糖代谢的基因缺乏特征描述,都使我们对果糖在神经能量代谢中的生理作用的理解变得复杂。最近一项对小脑的神经代谢研究表明,浦肯野细胞中存在果糖代谢以及1-磷酸果糖途径特异性基因GLUT5(葡萄糖转运蛋白5)和己酮糖激酶(khk)的共表达,这表明这是特定神经元中的一条活跃途径?与此同时,对膳食果糖迅速增加的担忧,尤其是在儿童中,提高了人们对果糖在体内如何代谢以及高果糖饮食可能产生何种影响的认识。在这方面,建立细胞和分子研究以及对果糖在大脑中所起的重要和/或有害作用进行生理特征描述至关重要。本综述将特别参考小脑来讨论大脑中果糖代谢的状况以及不同途径的生理作用。