Manipulation of growth in pigs through treatment of the neonate with clenbuterol and somatotropin1

Abstract

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 Once the drugs were withdrawn at 40 d, the anabolic effect of pST gradually disappeared, so that the live weight of pST-treated and control pigs was identical at 168 d. Clenbuterol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.

BOARD-INVITED REVIEW: The biology and regulation of preadipocytes and adipocytes in meat animals1,2

“…Because subcutaneous, internal, seam, and intramuscular adipose tissue depots are all economically and physiologically important in meat animal production, deciphering the regulation of each adipose depot may lead to new strategies of animal production. However, it appears that not all adipose depots within or between animals are similarly maintained or regulated (Hood and Allen, 1973;Allen, 1976;Hood, 1982;Cianzio et al, 1985;May et al, 1995;Sillence et al, 2002;Albrecht et al, 2006;Fernyhough et al, 2007). This not only highlights the difficulties encountered in the thorough study of adipocytes, but also suggests that not all adipocytes are similar in form and function.…”

Novel strategies for tracing the exposure of meat cattle to illegal growth-promoters

“…Briefly, the use of analogues of known compounds -also known as designer drugs-or of molecules not subjected to routine controls, either of natural origin or licensed for the use in non-EU countries, is believed to play a critical role to explain the failure in detecting such illegal treatments. In this respect, somatotropin (GH) is reported to be used also in meat cattle, alone or in association with a β-agonist because of the GH-mediated up-regulation of β-adrenoceptors occurring in certain species (Sillence, 2002) and organic chromium may be employed to improve the fat:lean ratio (Sillence, 2004). Recent telling examples in the bovine species are the suspected/potential misuse of either cyproheptadine, a cheap and easily available piperidine antihistaminic which is attractive to farmers since it increases appetite through its anti-serotoninergic effect on brain 5-HT2 receptors and displays sedative effects (Feás et al, 2009), or of ecdysteroids, a class of steroids acting as moulting hormones in arthropods but also found in many plants (Destrez et al, 2008).…”

Turning fat into muscle: can this be an alternative to anti‐obesity drugs such as semaglutide?

“…However, the aforementioned Akt1 mice had ≈50% less inguinal and subcutaneous fat than wild‐type mice (Izumiya et al., 2008), and Mstn −/− A y /a mice had similarly less than ≈50% inguinal, epididymal, parametrial and retroperitoneal fat than Mstn +/+ A y /a mice (McPherron & Lee, 2002). Moreover, a combinatorial treatment of clenbuterol and porcine growth hormone reduced carcass fat in pigs by 41% (Sillence et al., 2002). Whilst we admittedly are comparing apples with pears and whilst many anti‐obesity drug trials have not measured fat mass as an outcome, it seems that one might be able to achieve similar magnitudes of fat loss with treatments that stimulate global muscle hypertrophy (i.e.…”