LIPOLYTIC RESPONSES TO CATECHOLAMINES IN RACTOPAMINE-TREATED PIGS

Citation
Fr. Dunshea et al., LIPOLYTIC RESPONSES TO CATECHOLAMINES IN RACTOPAMINE-TREATED PIGS, Australian Journal of Agricultural Research, 49(5), 1998, pp. 875-881
Citations number
19
Categorie Soggetti
Agriculture
ISSN journal
00049409
Volume
49
Issue
5
Year of publication
1998
Pages
875 - 881
Database
ISI
SICI code
0004-9409(1998)49:5<875:LRTCIR>2.0.ZU;2-X
Abstract
The beta-agonist ractopamine (RAC) promotes protein deposition with li ttle effect on fat deposition in the pig. To assess whether the lack o f effect on fat deposition was due to changes in response to catechola mines, crossbred pigs with venous catheters were used to examine plasm a non-esterified fatty acid (NEFA) concentrations before and after int ravenous (i.v.) injections of the (beta(1)+beta(2))-agonist isoprotere nol and the beta(2)-agonist fenoterol during dietary RAC (0 or 20 mg/k g) treatment. In Expt 1, gilts received increasing i.v. doses of fenot erol [3, 9, 27, 81, and 243 mu g/kg bodyweight (BW)] on Day 34 and blo od samples were taken for metabolite analyses. The protocol was repeat ed on Day 36 but this time using increasing doses of isoproterenol (0. 11, 0.33, 1, 3, and 9 mu g/kg BW). Dietary RAC decreased basal NEFA co ncentrations but had no effect on plasma glucose concentrations. When the individual NEFA responses to fenoterol curves were fitted, the der ived values for maximal response (Rmax) suggested that there was no di fference between pigs fed 0 or 20 mg/kg RAC (1739 v. 1847 mu mol/L, P = 0.829). However, there was an almost 10-fold increase in the dose of fenoterol required to elicit a NEFA response 50% of Rmax (ED50) in RA C-fed pigs (11.6 v. 107.0 mu g/kg, P = 0.008). Intravenous fenoterol c hallenge increased plasma glucose linearly but this response was not a ltered by dietary RAG. In Expt 2, gilts received increasing i.v. doses of fenoterol (16, 80, and 400 mu g/kg BW) on Day 10 and blood samples were taken for metabolite analyses. The protocol was repeated on Day 11 but this time using increasing doses of isoproterenol (6.25, 32.5, and 162.5 mg/kg BW). The derived values for Rmax suggested that there was no effect of injected beta-agonist (2209 v. 2405 mu mol/L for feno terol and isoproterenol, respectively, P = 0.204) or dietary RAC (2251 v. 2363 mu mol/L for 0 or 20 mg/kg RAG, respectively, P = 0.448) on R max. However, the ED50 was significantly lower for isoproterenol than for fenoterol (14.1 v. 31.3 mu g/kg, P = 0.001) and was increased by d ietary RAC (18.6 v. 26.9 mu g/kg, P = 0.05), In conclusion, these data support the hypothesis that the lack of effect of dietary RAC on the rate of lipid deposition in the pig is due to a desensitisation of adi pose tissue beta-adrenergic receptors-with no change in adipose tissue responsiveness.