Intestinal sphingolipid excretion associated with feeding of phytohemagglutinin lectin (Phaseolus vulgaris) to germ-free and conventional rats.
Intestinal sphingolipid excretion associated with feeding of phytohemagglutinin lectin (Phaseolus vulgaris) to germ-free and conventional rats.
复制标题
肠道鞘脂排泄与向无菌和常规大鼠饲喂植物血凝素凝集素（菜豆）相关。
DOI：
10.1007/bf01053776
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发表时间：
1989
影响因子：
3
通讯作者：
Banwell,JG
中科院分区：
文献类型：
--
作者：
Larson,G;Falk,P;Howard,R;Banwell,JG
肠道鞘脂的粪便中的无菌和传统的大鼠进行了分析，在一个完整的定义的饮食含有植物血凝素凝集素（PHA）从红芸豆（菜豆）作为1%的膳食蛋白质相比，酪蛋白喂养的控制对喂养。与对照组相比，饮食中的植物血凝素增加了鞘磷脂（无菌大鼠为18倍，传统大鼠为20倍）、非酸性鞘糖脂（无菌大鼠为3.5倍，传统大鼠为9倍）以及无菌大鼠神经节苷脂（2.5倍）的总粪便排泄量。对于无菌大鼠，非酸性糖脂的增加归因于凝集素严格作用于小肠粘膜，而对于常规大鼠，也观察到作用于大肠粘膜。无菌大鼠粪便神经节苷脂的增加主要是由于N-乙酰神经氨酰-乳糖神经酰胺（一种仅限于十二指肠、空肠上部和大肠上皮细胞的神经节苷脂）的排泄增加。在无菌大鼠中观察到的对糖脂排泄的影响和在常规动物中观察到的相当类似的影响表明，饮食PHA的影响是直接由于PHA与肠细胞刷状缘膜结合引起的影响，而不是由于管腔微生物菌群增加引起的继发性影响。
Intestinal sphingolipids of feces of germ-free and conventional rats were analyzed during the pair feeding of a complete defined diet containing phytohemagglutinin lectin (PHA) from red kidney beans (Phaseolus vulgaris) as 1% dietary protein in comparison to casein fed controls. Phytohemagglutinin in the diet increased the total fecal excretion of sphingomyelins (18-fold for germ-free and 20-fold for conventional rats), of non-acid glycosphingolipids (3.5-fold for germ-free and 9-fold for conventional rats) and also of the gangliosides (2.5-fold) for the germ-free rats compared to controls. For germ-free rats the increase of non-acid glycolipids was ascribed to an effect of the lectin strictly on the small intestinal mucosa, while for conventional rats an effect was seen also on the large intestinal mucosa. Increase of fecal gangliosides of germ-free rats was due mainly to an increased excretion ofN-acetylneuraminosyl-lactosylceramide, a ganglioside species restricted to epithelial cells of duodenum, of upper jejunum and of large intestines. The effects on glycolipid excretion observed in germ-free rats and the rather similar effects seen in conventional animals suggested that the influence of dietary PHA was due directly to effects elicited by PHA binding to the enterocyte brush border membrane and not to secondary effects induced by increase in the luminal microflora.