Effects of dexamethasone and colostrum feeding on mRNA levels and binding capacities of beta-adrenergic receptors in the liver of neonatal calves.
Glucocorticoids increase plasma glucose concentrations in neonatal calves, but not hepatic gluconeogenic enzyme mRNA levels and activities. Catecholamines, too, enhance plasma glucose levels and regulate hepatic glucose metabolism. We have measured hepatic mRNA levels of beta-adrenergic receptors and beta-adrenergic receptor binding in neonatal calves on day 5 of life. Calves were fed either colostrums (C) or an isoenergetic milk-based formula (F), and in each feeding group, half of the calves were treated with dexamethasone (DEXA; 30 microg/(kg body weightday)). Abundance of mRNA was highest (P < 0.01) for beta2-adrenergic receptors and was higher (P < 0.01) for beta1- than for beta3-adrenergic receptors. DEXA treatment decreased (P < 0.05) beta1- and beta2-adrenergic receptor mRNA levels. Beta3-adrenergic receptor mRNA levels were higher (P < 0.05) in colostrum- than in formula-fed calves. Competitive binding revealed highest affinities for alprenolol, propranolol (both beta1- and beta2-antagonists), and ICI-188,551 (beta2-antagonist), which did not significantly differ from each other. Atenolol (beta1-antagonist) up to 10(-5) M did not displace (3H)-CGP-12177 from receptors. Competitive binding for adrenaline was best fitted by a two-receptor model. DEXA decreased (P < 0.05) (3H)-CGP-12177 binding capacities, whereas binding affinity of (3H)-CGP-12177 was not affected by DEXA or different feeding. Binding sites correlated positively with mRNA levels of beta2-adrenergic receptors (r = 0.56; P < 0.01). In conclusion, beta2-adrenergic receptors were the dominant subtype in the hepatic tissue. Feeding did not significantly affect beta2-adrenergic binding sites. However, DEXA decreased beta2-adrenergic binding sites and this was regulated at the transcriptional level.
Carron
J
J
Division of Nutrition and Physiology, Institute of Animal Genetics, Nutrition and Housing, Vetsuisse Faculty, University of Berne, CH-3012 Berne, Switzerland.
Morel
C
C
Blum
J W
JW
Hammon
H M
HM
D000319:Adrenergic beta-Antagonists / Q000378:metabolism; D000526:Alprenolol / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D001667:Binding, Competitive; D002417:Cattle / Q000378:metabolism*; D003126:Colostrum; D003907:Dexamethasone / Q000494:pharmacology; D004032:Diet; D005938:Glucocorticoids / Q000494:pharmacology*; D008099:Liver / Q000737:chemistry*; D016133:Polymerase Chain Reaction; D011412:Propanolamines / Q000378:metabolism; D011433:Propranolol / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis*; D011943:Receptors, Adrenergic, beta / Q000235:genetics / Q000378:metabolism*; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics / Q000378:metabolism; D022702:Receptors, Adrenergic, beta-3 / Q000235:genetics / Q000378:metabolism
D000319:Adrenergic beta-Antagonists; D005938:Glucocorticoids; D011412:Propanolamines; D012333:RNA, Messenger; D011943:Receptors, Adrenergic, beta; D018343:Receptors, Adrenergic, beta-2; D022702:Receptors, Adrenergic, beta-3; D003907:Dexamethasone; D000526:Alprenolol; D011433:Propranolol; C033394:CGP 12177