Fr. Dunshea et al., LIPOLYTIC RESPONSES TO CATECHOLAMINES IN RACTOPAMINE-TREATED PIGS, Australian Journal of Agricultural Research, 49(5), 1998, pp. 875-881
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.