Influence of spermine on intestinal maturation of the glycoprotein glycosylation process in neonatal rats

Previous work has shown an inverse evolution of the rat intestinal glycopro tein sialylation that decreases from birth to weaning and of fucosylation t hat increases markedly after weaning during postnatal development. At weani ng time, an increase in the intestinal level of polyamines (and especially that of spermine) was observed, owing partly to the higher level of spermin e found in solid food given to rats at this period in comparison with the l evel found in milk. To study the role of this polyamine as a possible matur ation factor of the glycoprotein glycosylation, suckling rats were treated for 4 days with spermine administered orally. This treatment allowed us to mimic the spermine increase that was observed naturally in rat small intest ine after weaning because, in intestines of spermine-treated suckling rats, spermine was the only polyamine to be increased and was at a level similar to that of weaned rats. Spermine treatment did not induce appreciable chan ges in sialyltransferase activity or in sialylation of the brush-border-mem brane glycoproteins. On the contrary, this treatment induced a rise in an a lpha-1,2-fucosyltransferase activity that was regulated at the transcriptio nal level, but not by its inhibitor (fuctinin), and no change in the availa bility of substrate (GDP-fucose). As a consequence of the increase in a: 1, 2-fucosyltransferase level and of the decrease in alpha-L-fucosidase level after treatment with spermine, several alpha-1,2-fucoproteins, naturally fo und in brush border membranes after weaning time, appeared precociously in these membranes after the treatment of the immature suckling rats. These re sults indicate that spermine is a maturation factor for the fucosylation of intestinal brush-border-membrane glycoproteins but not for their sialylati on, and that this polyamine might be implicated in the increased fucosylati on naturally occurring at weaning time during postnatal development.