Isoproterenol-mediated parotid gland hypertrophy is inhibited by effectors of 4 beta-galactosyltransferase.
Chronic administration of the beta-adrenergic receptor agonist isoproterenol results in parotid gland hypertrophy and hyperplasia. This physiological change in the gland has recently been reported to be accompanied by a dramatic increase in the rate of synthesis and accumulation of the enzyme 4 beta-galactosyltransferase. Here, isoproterenol-induced hypertrophy of the parotid gland is shown to be blocked by the introduction of the 4 beta-galactosyltransferase modifier protein alpha-lactalbumin and also by specific antiserum to bovine 4 beta-galactosyltransferase. Partial inhibition of gland enlargement was observed stereospecifically with UDP-galactose and with the competitive acceptor glycoprotein, ovalbumin, as well. These agents did not affect the induction by isoproterenol of the biosynthesis of the proline-rich proteins nor of 4 beta-galactosyltransferase. These agents also inhibited the incorporation of thymidine by isoproterenol-stimulated parotid cells in culture.
D000818:Animals; D002478:Cells, Cultured; D002851:Chromatography, High Pressure Liquid; D004261:DNA Replication / Q000187:drug effects; D004789:Enzyme Activation; D005700:Galactosyltransferases / Q000378:metabolism*; D006984:Hypertrophy; D007545:Isoproterenol / Q000494:pharmacology*; D007788:Lactose Synthase / Q000378:metabolism*; D008297:Male; D010306:Parotid Gland / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains
D005700:Galactosyltransferases; D007788:Lactose Synthase; D007545:Isoproterenol