Manipulation of growth in pigs through treatment of the neonate with clenbuterol and somatotropin.

Neonatal pigs were treated with lipolytic agents to determine whether this would cause a long-term decrease in their ability to deposit fat, with a consequent increase in muscle growth and feed efficiency. Groups of 25 female piglets were given clenbuterol (100 microg/kg BW), porcine somatotropin (pST; 100 microg/kg BW), pST plus clenbuterol, or saline injections from 3 d to 40 d of age. Five piglets from each group were then slaughtered to determine body composition. Clenbuterol and pST both increased ADG up to weaning when given separately (24%, P < 0.05; 20%, P < 0.1 respectively) but did not reduce fat deposition. In contrast, pigs given clenbuterol plus pST showed no increase in ADG and a 41% reduction in carcass fat (P < 0.05). Clenbuterol caused a marked decrease in beta2-adrenoceptor density in porcine adipose tissue (P < 0.001) and skeletal muscle (P < 0.01). This effect was attenuated by concurrent pST treatment, which helps to explain the synergistic effect of these drugs on fat deposition. Once the drugs were withdrawn at 40 d, the anabolic effect of pST gradually disappeared, so that the live weight of pST-treated and control pigs was identical at 168 d. Clenbuterol withdrawal caused the rapid loss of extra weight gained, plus an additional 4 to 5 kg live weight that was never recovered. During the 4-wk finishing period there was an increase in feed intake in pigs that had previously undergone treatment with pST (23%, P < 0.1), with no increase in ADG, and so feed efficiency was impaired (P < 0.05). Pigs that were treated with pST plus clenbuterol showed no marked increase in feed intake during this period. Carcasses from clenbuterol-treated pigs tended to be leaner at 168 d, but there was no long-term effect of pST or the combined treatment on carcass composition. Overall, the treatment of neonatal pigs with repartitioning agents was counter-productive, due to the withdrawal effects of the beta-adrenefgic agonist and the delayed long-term effect of pST on feed intake.