Highly purified porcine growth hormone (pGH; USDA-B1) was administered by im injection (22 micrograms X kg body weight-1 X d-1) to rapidly growing Yorkshire barrows for 30 d. Growth hormone significantly increased growth rate (10%), feed efficiency (4%), cartilage growth and muscle mass. However, pGH did not affect carcass adipose tissue mass. Intramuscular lipid content of the longissimus was increased 50% by pGH administration. Plasma pGH concentration was elevated (7- to 11-fold) for 3 to 5 h post-injection. Chronic administration of pGH depressed pituitary GH content and concentration approximately 45%. No GH antibodies were detected in the plasma of GH-treated swine. Plasma somatomedin-C concentration was increased 55% by GH treatment 3 h post-injection. Plasma glucose and insulin concentrations were both significantly increased in GH-treated swine, suggesting that the animals had developed a state of insulin resistance. Plasma-free fatty acid concentration tended to be higher in GH-treated animals. Treatment of swine with pGH significantly decreased plasma blood urea nitrogen. Assessment of animal health during the trial and postmortem indicated that pGH administration did not have any adverse effects. In summary, treatment of young, rapidly growing swine with pGH stimulated growth performance without affecting animal health or inducing the production of GH antibodies.

This study was conducted to establish the extent to which different doses of pituitary porcine growth hormone (ppGH) increase pig growth performance. Pigs were treated daily for 11 wk with 0, 35 or 70 micrograms ppGH/kg BW. In addition, these effects were compared with those produced by treating pigs with 0, 35, 70 or 140 micrograms.kg BW-1.d-1 of a recombinantly derived analog of porcine growth hormone (rpGH). This analog lacks the first seven amino acids at the NH2 terminus. Growth rate was increased similarly by ppGH and rpGH (the maximal increase was 19%). Feed efficiency was improved by ppGH and rpGH (the maximal response was 25%). This improvement in feed efficiency was associated with a decrease in feed intake (17% with the largest dose of rpGH). Both ppGH and rpGH decreased adipose tissue growth and increased muscle mass. Carcass lipid was decreased by 68% in pigs treated with the largest dose of rpGH. The recombinant pGH analog appeared to be less potent than ppGH in decreasing adipose tissue growth rate. All other parameters measured, however, indicated that rpGH mimicked the biological effects of ppGH (including binding to pig liver membranes and induction of insulin-like growth factor I production). Sensory panel evaluations indicated that neither ppGH nor rpGH affected pork palatability. Larger doses of pGH (greater than 70 micrograms/kg BW) adversely affected pig mobility. This impairment in mobility appears to be due to osteochondrosis. Our findings establish that the rpGH analog is equipotent to ppGH in stimulating growth performance and that pigs can be treated without any significant adverse effects when they are treated with less than 70 micrograms of pGH.kg BW-1.d-1.

The current study was undertaken to determine the effects of human growth hormone-releasing factor [hpGRF-(1-44)-NH2] on growth performance in pigs and whether this response was comparable to exogenous porcine growth hormone (pGH) treatment. Preliminary studies were conducted to determine if GRF increased plasma GH concentration after iv and im injection and the nature of the dose response. Growth hormone-releasing factor stimulated the release of pGH in a dose-dependent fashion, although the individual responses varied widely among pigs. The results from the im study were used to determine the dose of GRF to use for a 30-d growth trial. Thirty-six Yorkshire-Duroc barrows (initial wt 50 kg) were randomly allotted to one of three experimental groups (C = control, GRF and pGH). Pigs were treated daily with 30 micrograms of GRF/kg body weight by im injection in the neck. Pigs treated with pGH were also given 30 micrograms/kg body weight by im injection. Growth rate was increased 10% by pGH vs C pigs (P less than .05). Growth rate was not affected by GRF; however, hot and chilled carcass weights were increased 5% vs C pigs (P less than .05). On an absolute basis, adipose tissue mass was unaffected by pGH or GRF. Carcass lipid (percent of soft-tissue mass) was decreased 13% by GRF (P less than .05) and 18% by pGH (P less than .05). Muscle mass was significantly increased by pGH but not by GRF. There was a trend for feed efficiency to be improved by GRF; however, this was not different from control pigs. In contrast, pGH increased feed efficiency 19% vs control pigs (P less than .05). Chronic administration of GRF increased anterior pituitary weight but did not affect pituitary GH content or concentration. When blood was taken 3 h post-injection, both GRF- and pGH-treated pigs had lower blood-urea nitrogen concentrations. Serum glucose was significantly elevated by both GRF and pGH treatment. This was associated with an elevation in serum insulin. These results indicate that increasing the GH concentration in blood by either exogenous GH or GRF enhances growth performance. The effects of pGH were more marked than for GRF. Further studies are needed to determine the optimal dose of GRF to administer in growth trials and the appropriate pattern of GRF administration in order to determine whether GRF will enhance pig growth performance to the extent that exogenous pGH does.

No abstract