title: Ontogenesis of mRNA levels and binding sites of hepatic alpha-adrenoceptors in young cattle.
abstract: Catecholamines affect hepatic glucose production through (alpha- and beta2-) adrenoceptors (AR). We studied mRNA abundance and binding of hepatic alpha-AR in pre-term (P0) calves and in full-term calves at day 0 (F0), day 5 (F5) and day 159 (F159) to test the hypothesis that gene expression and numbers of hepatic alpha-AR in calves are influenced by age and associated with beta2-AR and selected traits of glucose metabolism. mRNA levels of alpha1- and alpha2-AR were measured by real time RT-PCR. alpha1- and alpha2-AR numbers (maximal binding, Bmax) were determined by saturation binding of (3H)-prazosin and (3H)-RX821002, respectively. alpha1- and alpha2-AR subtypes were evaluated by competitive binding. alpha1A-AR mRNA levels were lower in P0 than in F0, F5 and F159 and alpha(2AD)-AR mRNA levels were lower in F159 than in P0, F0 and F5, while alpha2C-AR mRNA levels increased from P0 and F0 to F5 and F159. Bmax of alpha1-AR increased from P0 to F5, then decreased in F159. Bmax of alpha2-AR decreased from F0 to F159. Bmax of alpha1-AR was positively associated with mRNA levels of alpha1A-AR (r = 0.7), Bmax of beta2-AR (r = 0.5) and negatively with hepatic glycogen content (r = -0.6). Bmax of alpha2-AR was negatively associated with Bmax of beta2-AR (r = -0.4). In conclusion, mRNA levels and binding sites of alpha1- and alpha2-AR in calves exhibited developmental changes and were negatively associated with hepatic glycogen content.
authors.affiliation: Division of Nutrition and Physiology, Institute of Animal Genetics, Nutrition and Housing, Vetsuisse Faculty, University of Bern, CH-3012 Bern, Switzerland.
authors.forename: E C
authors.initials: EC
authors.lastname: Ontsouka
authors.forename: Y
authors.initials: Y
authors.lastname: Zbinden
authors.forename: H M
authors.initials: HM
authors.lastname: Hammon
authors.forename: J W
authors.initials: JW
authors.lastname: Blum
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001667:Binding, Competitive; D001786:Blood Glucose / Q000378:metabolism; D002417:Cattle / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D005260:Female; D006003:Glycogen / Q000097:blood; D019329:Idazoxan / Q000031:analogs & derivatives / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D010728:Phosphoenolpyruvate / Q000378:metabolism; D011224:Prazosin / Q000494:pharmacology; D011247:Pregnancy; D011766:Pyruvate Carboxylase / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000317:Adrenergic alpha-Antagonists; D001786:Blood Glucose; D012333:RNA, Messenger; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D010728:Phosphoenolpyruvate; D006003:Glycogen; C058525:2-methoxyidazoxan; D011766:Pyruvate Carboxylase; D011224:Prazosin; D019329:Idazoxan