Lipolytic responses to catecholamines in ractopamine-treated pigs

Abstract

The β-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 catecholamines, crossbred pigs with venous catheters were used to examine plasma non-esterified fatty acid (NEFA) concentrations before and after intravenous (i.v.) injections of the (β₁+β₂)-agonist isoproterenol and the β₂-agonist fenoterol during dietary RAC (0 or 20 mg/kg) treatment. In Expt 1, gilts received increasing i.v. doses of fenoterol [3, 9, 27, 81, and 243 µg/kg bodyweight (BW)] on Day 34 and blood samples were taken for metabolite analyses. The protocol was repeated on Day 36 but this time using increasing doses of isoproterenol (0·11, 0·33, 1, 3, and 9 µg/kg BW). Dietary RAC decreased basal NEFA concentrations but had no effect on plasma glucose concentrations. When the individual NEFA responses to fenoterol curves were fitted, the derived values for maximal response (Rmax) suggested that there was no difference between pigs fed 0 or 20 mg/kg RAC (1739 v. 1847 µmol/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 RAC-fed pigs (11·6 v. 107·0 µg/kg, P = 0·008). Intravenous fenoterol challenge increased plasma glucose linearly but this response was not altered by dietary RAC. In Expt 2, gilts received increasing i.v. doses of fenoterol (16, 80, and 400 µg/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 β-agonist (2209 v. 2405 µmol/L for fenoterol and isoproterenol, respectively, P = 0·204) or dietary RAC (2251 v. 2363 µmol/L for 0 or 20 mg/kg RAC, respectively, P = 0·448) on Rmax. However, the ED₅₀ was significantly lower for isoproterenol than for fenoterol (14·1 v. 31·3mg/kg, P = 0·001) and was increased by dietary RAC (18·6 v 26·9 µg/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 adipose tissue β-adrenergic receptors with no change in adipose tissue responsiveness.