title: Alpha-lactalbumin acts as a bimodal regulator of rat parotid acinar cell growth.
abstract: Isoproterenol, a beta-adrenergic receptor agonist, causes hypertrophy and hyperplasia of the rat parotid gland. The stimulation of parotid acinar cells to a growth phase is accompanied by a cell surface localization of the enzyme 4 beta-galactosyltransferase. Alpha-lactalbumin, a specific modifier protein for 4 beta-galactosyltransferase, when given subsequent to the initiation of isoproterenol treatment and the commencement of parotid enlargement, resulted in a termination of gland hypertrophy and DNA synthesis. Gland size did not, however, return to control levels with the continued injection of isoproterenol and alpha- lactalbumin. In contrast, the injection of alpha-lactalbumin in neonatal rats (7-14 days post-partum) stimulated parotid gland hypertrophy and DNA synthesis. This treatment also lead to the precocious expression of the major parotid gland salivary enzyme, amylase.
mesh_terms: D000367:Age Factors; D000681:Amylases / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D002462:Cell Membrane / Q000201:enzymology; D005700:Galactosyltransferases / Q000502:physiology*; D006984:Hypertrophy; D007545:Isoproterenol / Q000494:pharmacology*; D007768:Lactalbumin / Q000502:physiology*; D010306:Parotid Gland / Q000254:growth & development*; D051381:Rats; D006022:beta-N-Acetylglucosaminylglycopeptide beta-1,4-Galactosyltransferase / Q000502:physiology*
chemical_list: D007768:Lactalbumin; D005700:Galactosyltransferases; D006022:beta-N-Acetylglucosaminylglycopeptide beta-1,4-Galactosyltransferase; D000681:Amylases; D007545:Isoproterenol