Köttgen E, Beiswenger M, James L F, Bauer C
Institut für Klinische Chemie und Klinische Biochemie, Universitätsklinikum Rudolf Virchow, Berlin, Federal Republic of Germany.
Gastroenterology. 1988 Jul;95(1):100-6. doi: 10.1016/0016-5085(88)90296-x.
Simultaneous feeding of gliadin and swainsonine, an inhibitor of alpha-D-mannosidases, in rats disturbed enterocytic maturation as shown by a marked loss of activities of alkaline phosphatase and gamma-glutamyltransferase. Morphologically, simultaneous treatment with gliadin and swainsonine caused destruction and decreased density of microvilli, as shown by electron microscopy. Neither gliadin nor swainsonine when given alone had significant effects on enterocytic enzyme activities or enterocytic morphology. Binding of enterocytic glycoproteins to both gliadin-Sepharose and concanavalin A-Sepharose was significantly increased in rats treated with swainsonine. Because swainsonine causes the formation of hybrid-type oligosaccharides with a high binding affinity to mannose-specific lectins, the observed alterations of enterocytic maturation and morphology are presumably caused by the increased binding of gliadin to enterocytic glycoproteins. A possible analogy in the etiology of celiac disease is discussed.
在大鼠中同时喂食麦醇溶蛋白和α-D-甘露糖苷酶抑制剂苦马豆素，会干扰肠细胞成熟，表现为碱性磷酸酶和γ-谷氨酰转移酶活性显著丧失。从形态学上看，电子显微镜显示，同时用麦醇溶蛋白和苦马豆素处理会导致微绒毛遭到破坏且密度降低。单独给予麦醇溶蛋白或苦马豆素对肠细胞酶活性或肠细胞形态均无显著影响。在用苦马豆素处理的大鼠中，肠细胞糖蛋白与麦醇溶蛋白-琼脂糖和伴刀豆球蛋白A-琼脂糖的结合均显著增加。由于苦马豆素会导致形成与甘露糖特异性凝集素具有高结合亲和力的杂合型寡糖，因此观察到的肠细胞成熟和形态改变可能是由麦醇溶蛋白与肠细胞糖蛋白结合增加所致。本文讨论了乳糜泻病因学中可能存在的类似情况。
