Gréco S, Niepceron E, Hugueny I, George P, Louisot P, Biol M C
Université Claude Bernard Lyon 1, BP 12, 69600, France.
J Nutr. 2001 Jul;131(7):1890-7. doi: 10.1093/jn/131.7.1890.
This study considered the role of dietary polyamines in the maturation of intestinal glycoprotein galactosylation during postnatal development. In the rat small intestine, O-glycan: beta-1,3-galactosyltransferase and N-glycan: beta-1,4-galactosyltransferase are, respectively, involved in the glycan chain biosynthesis of mucins and of glycoproteins in the brush border membranes. Their activities increase significantly at weaning, in parallel with a rise in the intestinal content of spermidine and spermine (as determined by high performance liquid chromatography) and in proportion to the polyamine increase in food intake. The oral ingestion of spermidine or spermine (at 0.4 micromol/g body) by immature suckling rats for 4 d reproduced the levels of spermine and spermidine in their intestines at the time of weaning and induced precocious and significant rises in O-glycan: and N-glycan: galactosyltransferase activities to those normally found after weaning. In parallel, more galactose residues (detected in the complex oligosaccharide chains of glycoproteins by specific lectins after electrophoresis and transfer to nitrocellulose membranes) were observed in the brush border membranes of spermidine- and spermine-treated rats. In contrast, the ingestion of putrescine or ornithine had no effect. Diets with different levels of polyamines (milks and commercial diet), when given at weaning, induced variable evolutions of the galactosylation process, partly in relation to the amounts of polyamines ingested. These results indicate that spermidine and spermine are maturation factors that can reproduce, in immature rats, the same increase in intestinal glycoprotein galactosylation that is normally observed during weaning. They also suggest that the maturation of glycoprotein galactosylation may be a multifactorial event in which spermidine and spermine are both involved.
本研究探讨了膳食多胺在出生后发育过程中肠道糖蛋白半乳糖基化成熟中的作用。在大鼠小肠中,O-聚糖:β-1,3-半乳糖基转移酶和N-聚糖:β-1,4-半乳糖基转移酶分别参与粘蛋白和刷状缘膜中糖蛋白的聚糖链生物合成。它们的活性在断奶时显著增加,同时精胺和亚精胺的肠道含量上升(通过高效液相色谱法测定),且与食物摄入量中多胺的增加成比例。未成熟的乳鼠口服亚精胺或精胺(0.4 μmol/g体重)4天,可使断奶时肠道中的精胺和亚精胺水平恢复,并使O-聚糖和N-聚糖半乳糖基转移酶活性提前且显著升高至断奶后正常水平。同时,在经亚精胺和精胺处理的大鼠刷状缘膜中观察到更多的半乳糖残基(通过电泳并转移至硝酸纤维素膜后,用特异性凝集素在糖蛋白的复合寡糖链中检测到)。相比之下,摄入腐胺或鸟氨酸则没有影响。断奶时给予不同多胺水平的饮食(牛奶和商业饮食),会导致半乳糖基化过程出现不同的变化,部分与摄入的多胺量有关。这些结果表明,亚精胺和精胺是成熟因子,可在未成熟大鼠中重现断奶期间正常观察到的肠道糖蛋白半乳糖基化的相同增加。它们还表明,糖蛋白半乳糖基化的成熟可能是一个多因素事件,亚精胺和精胺均参与其中。