Thomson A B, Wild G
Division of Gastroenterology, University of Alberta, Edmonton, Canada.
Dig Dis Sci. 1997 Mar;42(3):453-69. doi: 10.1023/a:1018807120691.
Why is it important to understand the mechanisms controlling intestinal adaptation? There are two major answers to this question. Firstly, in establishing the cellular and molecular events associated with intestinal adaptation, we will formulate a general framework that may be applied to the understanding of adaptation of other cell membranes. For example, alterations in the synthesis of glucose carriers and their subsequent insertion into membranes may alter sugar entry across the intestinal brush border membrane (BBM) using the sodium-dependent D-glucose transporter, SGLT1, or the BBM sodium-independent facultative fructose transporter, GLUT5, and may alter facilitated sugar exit across the basolateral membrane (BLM) using GLUT2. The precise role of transcriptional and translational processes in the up- or down-regulation of sugar transport requires further definition. Alterations in enterocyte microsomal lipid metabolic enzyme expression occurring during the course of intestinal adaptation will direct the synthesis of lipids destined for trafficking to the BBM and BLM domains of the enterocyte. This will subsequently alter the passive permeability properties of these membranes and ultimately influence lipid absorption. Therefore, establishing the physiological, cellular and molecular mechanisms of adaptation in the intestine will define principles that may be applied to other epithelia. Secondly, enterocyte membrane adaptation is subject to dietary modification, and these may be exploited as a means to enhance a beneficial or to reduce a detrimental aspect of the intestinal adaptive process in disease states. Alterations in membrane function occur in association with changes in dietary lipids, and these are observed in a variety of cells and tissues including lymphocytes, testes, liver, adipocytes, nerve tissue, nuclear envelope and mitochondria. Therefore, the elucidation of the mechanisms of intestinal adaptation and the manner whereby dietary manipulation modulates these processes affords the future possibility of dietary engineering aimed at using food as a therapeutic agent. It is hoped this approach will form the centerpiece for future investigation that would focus on disease prevention, as well as on the development of better therapeutic strategies to prevent the development or to treat the complications of conditions such as diabetes mellitus, obesity, hyperlipidemia and inflammatory bowel diseases. This review deals with the physiology of glucose transport with specific emphasis on transporters of the brush border membrane (BBM) and the basolateral membrane (BLM). On the BBM the sodium (Na)/glucose transporters (SGLT1 and SGLT2), the Na-independent transporter (GLUT5), and on the BLM the hexose transporter (GLUT2) are discussed. The molecular biology of these transporters is also reviewed.
为什么了解控制肠道适应的机制很重要?这个问题主要有两个答案。首先,在确定与肠道适应相关的细胞和分子事件时,我们将构建一个通用框架,该框架可能适用于理解其他细胞膜的适应过程。例如,葡萄糖载体合成的改变以及它们随后插入膜中,可能会改变通过钠依赖性D-葡萄糖转运蛋白SGLT1或肠刷状缘膜(BBM)钠非依赖性兼性果糖转运蛋白GLUT5跨肠刷状缘膜(BBM)的糖进入,并且可能会改变通过GLUT2跨基底外侧膜(BLM)的易化糖输出。转录和翻译过程在糖转运上调或下调中的精确作用需要进一步明确。肠道适应过程中发生的肠上皮细胞微粒体脂质代谢酶表达的改变,将指导注定要运输到肠上皮细胞BBM和BLM结构域的脂质合成。这随后将改变这些膜的被动通透性特性,并最终影响脂质吸收。因此,确定肠道适应的生理、细胞和分子机制将定义可应用于其他上皮细胞的原则。其次,肠上皮细胞膜适应会受到饮食调整的影响,这些调整可被用作增强有益方面或减少疾病状态下肠道适应过程中有害方面的一种手段。膜功能的改变与饮食脂质的变化相关,并且在包括淋巴细胞、睾丸、肝脏、脂肪细胞、神经组织、核膜和线粒体在内的各种细胞和组织中都可观察到。因此,阐明肠道适应机制以及饮食操纵调节这些过程的方式,为未来将食物用作治疗剂的饮食工程提供了可能性。希望这种方法将成为未来研究的核心,该研究将专注于疾病预防以及开发更好的治疗策略,以预防诸如糖尿病、肥胖症、高脂血症和炎症性肠病等病症的发展或治疗其并发症。本综述论述了葡萄糖转运的生理学,特别强调了刷状缘膜(BBM)和基底外侧膜(BLM)的转运蛋白。在BBM上,讨论了钠(Na)/葡萄糖转运蛋白(SGLT1和SGLT2)、钠非依赖性转运蛋白(GLUT5),在BLM上,讨论了己糖转运蛋白(GLUT2)。还综述了这些转运蛋白的分子生物学。