Department of Biochemistry, Punjab University, Chandigarh 160014, India.
Alcohol. 2010 Sep;44(6):515-22. doi: 10.1016/j.alcohol.2010.07.008. Epub 2010 Aug 13.
Ethanol ingestion is well known to induce morphological and biochemical changes in intestine and is responsible for intestinal dysfunctions. Luminal surface of enterocytes is rich in glycolipids, but the effects of ethanol ingestion on membrane glycolipids are not well characterized. In the present study, rats were given 1 mL of 30% ethanol daily for 15, 25, 35, and 56 days. Ethanol feeding for 15 days did not affect glycolipid pattern in microvillus membranes, but the levels of cerebrosides (glucosylceramide, lactosylceramide, globotriasyloceramide) were enhanced in rats fed with ethanol for 35 or 56 days compared with controls. In contrast, the content of fucolipids and gangliosides was reduced in rats on ethanol ingestion for 35 or 56 days. The observed changes in membrane glycolipids were substantiated using biotinylated lectins Jacalin (affinity for N-acetylgalactosamine) and Aleuria aurantia (affinity for α-l-fucose). The incorporation of [(14)C]-mannose and [(14)C]-glucosamine revealed an increase (P<.01) in glucosamination and reduction (P<.01) in mannosylation of glycolipids from ethanol-fed rats for 45 days compared with controls. These findings were further characterized by autoradiography of the glycolipids separated on thin layer chromatograms. These findings indicate that ethanol ingestion modulates the glycolipids composition of brush borders, resulting in generalized aberration of intestinal glycosylation in chronic alcoholism in rats.
乙醇摄入众所周知会引起肠的形态和生化变化，并导致肠道功能障碍。肠上皮细胞的腔面富含糖脂，但乙醇摄入对膜糖脂的影响尚未得到很好的描述。在本研究中，大鼠每天给予 1 毫升 30%的乙醇，持续 15、25、35 和 56 天。乙醇喂养 15 天不会影响微绒毛膜中的糖脂模式，但与对照组相比，乙醇喂养 35 或 56 天的大鼠脑苷脂（葡萄糖神经酰胺、乳糖神经酰胺、Globotriasyloceramide）水平升高。相比之下，在 35 或 56 天的乙醇摄入大鼠中，岩藻糖脂和神经节苷脂的含量减少。使用生物素化凝集素 Jacalin（对 N-乙酰半乳糖胺的亲和力）和 Aleuria aurantia（对α-L-岩藻糖的亲和力）证实了膜糖脂的观察到的变化。[(14)C]-甘露糖和[(14)C]-葡萄糖胺的掺入表明，与对照组相比，45 天的乙醇喂养大鼠的糖脂糖基化（P<.01）增加，甘露糖基化（P<.01）减少。这些发现通过薄层层析分离的糖脂的放射自显影进一步得到了表征。这些发现表明，乙醇摄入调节刷状缘的糖脂组成，导致大鼠慢性酒精中毒中肠道糖基化的普遍异常。
