Glucocorticoid-induced maturation of glycoprotein galactosylation and fucosylation processes in the rat small intestine.
We determined the role of glucocorticoids in the maturation of glycoprotein galactosylation and fucosylation processes in the rat small intestine during postnatal development. Treatment of suckling rats with hydrocortisone (HC) increased activities of an O-glycan: galactosyltransferase, and of an alpha-1,2-fucosyltransferase, through transcriptional regulation of the FTB gene. The activities of a fucosyltransferase inhibitor and of the enzymes responsible for the synthesis and degradation of GDP-fucose were unaffected by the treatment, whereas a fall in the activity of alpha-L-fucosidase was observed. These changes were accompanied by the precocious appearance of alpha-1,2-fucose residues in complex glycan chains of brush-border membrane glycoproteins that normally appear after weaning, and with a trend to increase in alpha-1,2-fucose residues in mucins. Thus, treatment of suckling rats with hydrocortisone speeds up the maturation of glycoprotein galactosylation and fucosylation processes in the small intestine. The delayed increase in glucocorticoid levels induced by prolonged nursing, or the suppression of glucocorticoids by adrenalectomy (AD) before the normal rise in the hormone, both induced a delay in the increases in activities of the O-glycan: galactosyltransferase and alpha-1,2-fucosyltransferase observed normally after glucocorticoid enhancement. Thus, glucocorticoids might play at least a partial role in the maturation of glycoprotein glycosylation observed at weaning.
Département de Biochimie, Faculté de Médecine Lyon-Sud, Unité INSERM 189-SDI CNRS, BP 12, 69600 Oullins, France. biol@lyon-sud.univ-lyon1.fr
Marie-Claire
MC
Biol-N'garagba
Elodie
E
Niepceron
Bruno
B
Mathian
Pierre
P
Louisot
D000818:Animals; D015152:Blotting, Northern; D003345:Corticosterone / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005643:Fucose / Q000378:metabolism*; D005647:Fucosyltransferases / Q000378:metabolism; D005690:Galactose / Q000378:metabolism*; D005700:Galactosyltransferases / Q000378:metabolism; D005786:Gene Expression Regulation; D005938:Glucocorticoids / Q000494:pharmacology*; D006023:Glycoproteins / Q000378:metabolism*; D006727:Hormone Antagonists / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology; D007421:Intestine, Small / Q000187:drug effects* / Q000378:metabolism*; D015735:Mifepristone / Q000494:pharmacology; D009077:Mucins / Q000378:metabolism / Q000494:pharmacology; D012313:RNA / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013347:Subcellular Fractions; D013552:Swine; D013997:Time Factors; D014886:Weaning
D005938:Glucocorticoids; D006023:Glycoproteins; D006727:Hormone Antagonists; D009077:Mucins; D005643:Fucose; D015735:Mifepristone; D012313:RNA; D005647:Fucosyltransferases; D005700:Galactosyltransferases; D003345:Corticosterone; D006854:Hydrocortisone; D005690:Galactose