Implication of insulin and nutritional factors in the regulation of intestinal galactosyltransferase activity during postnatal development

In the rat small intestine, galactosyltransferases are the enzymes implicat ed in the biosynthesis of glycoproteins of the brush-border membranes and m ucins. During postnatal development, the circulating insulin level increase d at weaning in parallel with the activities of intestinal galactosyltransf erases on O-glycans and N-glycans. This study deals with the role of insuli n in the regulation of galactosyltransferase activities during postnatal de velopment. The treatment: of immature suckling rats with insulin induced a precocious increase in the activities of the O-glycan and N-glycan galactos yltransferases, partly reproducing the increase in galactosyltransferase ac tivity normally found at weaning, since the O-glycan galactosyltransferase activity increased more quickly then the N glycan galactosyltransferase act ivity. The sensitivity of the two galactosyltransferase activities to insul in disappeared after weaning, a period when drastic diet changes occur. In 22-day-old rats submitted to prolonged nursing thigh-fat diet), the activit ies of the O-glycan and N-glycan galactosyltransferases were lower than tho se found in age-matched normally weaned rats (high-carbohydrate diet), indi cating a delay In the maturation of the intestine of prolonged-nursing rats . The circulating insulin level of these animals stayed lower than that of the age-matched weaned rats. When the prolonged-musing animals were treated with insulin, the O-glycan and N-glycan galactosyltransferase activities r eached revels similar to those of the weaned rats. These observations sugge st that Insulin is one of the maturation factors for intestinal glycoprotei n galactosylation and may be partly responsible for the natural enhancement of intestinal galactosyltransferase activities observed during postnatal d evelopment in relation to the dietary changes at weaning. Copyright (C) 200 0 by W.B. Saunders Company.