title: Responses to homeostatic signals in ractopamine-treated pigs.
abstract: The beta-agonist ractopamine (RAC) promotes protein deposition with little effect on fat deposition in the pig. To assess whether the lack of effect on fat deposition was due to changes in response to homeostatic signals, eight crossbred gilts (73 kg body weight (BW)) with venous catheters were used to examine plasma metabolite and hormone concentrations before and after intravenous injections of insulin and the beta 2-agonist fenoterol during dietary RAC (0 or 20 mg/kg) treatment. Pigs received intravenous challenges of insulin (1 microgram/kg BW) on days 3, 9 and 23 and fenoterol (2 micrograms/kg BW) on days 4, 10 and 24 of treatment. RAC was then withdrawn from the diet and insulin and fenoterol challenges were repeated 6 and 7 d later respectively. Blood samples for the determination of metabolite and hormone concentrations were taken at -30, -20, -10, -1, 2.5, 5, 10, 20, 30, 45, 60 and 120 min relative to the challenges. Dietary RAC decreased basal plasma insulin concentrations but had no effect on plasma glucose or non-esterified fatty acids (NEFA). Hypoglycaemic responses to insulin were not affected by RAC while the anti-lipolytic effects of insulin tended to be augmented. Dietary RAC decreased the lipolytic response to fenoterol, this being evident after 4 d treatment. Hypoglycaemic response to fenoterol was not changed whereas the hyperinsulinaemic response to fenoterol was attenuated by dietary RAC. Previous treatment with RAC did not influence basal hormone and metabolite concentrations or responses to homeostatic signals during the withdrawal period. While these results suggest little change in glucose metabolism, the de-sensitization of adipose tissue beta-adrenergic receptors is consistent with the observations that dietary RAC has little effect on the rate of fat deposition in the growing pig.
authors.affiliation: Victorian Institute of Animal Science, Werribee, Australia.
authors.forename: F R
authors.initials: FR
authors.lastname: Dunshea
authors.forename: R H
authors.initials: RH
authors.lastname: King
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000318:Adrenergic beta-Agonists / Q000008:administration & dosage*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004032:Diet; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005280:Fenoterol; D006133:Growth Substances / Q000008:administration & dosage*; D006706:Homeostasis / Q000187:drug effects*; D007275:Injections, Intravenous; D007328:Insulin / Q000097:blood; D008066:Lipolysis / Q000187:drug effects; D010627:Phenethylamines / Q000008:administration & dosage*
chemical_list: D000318:Adrenergic beta-Agonists; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D006133:Growth Substances; D007328:Insulin; D010627:Phenethylamines; D005280:Fenoterol; C060897:ractopamine