Purified chicken growth hormone (GH) and a human pancreatic GH-releasing hormone increase body weight gain in chickens.

Purified chicken GH (cGH) and a synthetic human GH-releasing hormone (hpGRF) were tested for the ability to improve growth performance in chickens. Purified cGH was given to 4-week-old cockerels at 5, 10, and 50 micrograms/day for 14 days via daily iv injection. Body weights of chickens receiving 5 and 10 micrograms/day cGH were significantly increased at 6 days by 13.5% and 11.2%, respectively, relative to control values. At 14 days, body weights averaged 8.1% and 7.7% greater than controls, but these values were not statistically significant. There was a slight stimulation of body weight gain in chickens receiving 50 micrograms/day cGH. In general, cGH produces a transient stimulation of body weight gain in chickens. hpGRF was also given to 4-week-old cockerels for 14 days via daily iv injection at 0.1, 1.0, and 10.0 micrograms/day. hpGRF at 0.1 microgram/bird daily increased body weight on day 14 (9.1% over the control value). The stimulating effects of hpGRF on body weight are also transient. The effects of cGH on serum somatomedin-C (SM-C) were examined. Serum SM-C concentrations were significantly elevated 24 and 36 h after injection of cGH. In conclusion, purified cGH and hpGRF appear to have some growth-promoting activity. The stimulatory effect of hpGRF on weight gain may be mediated via GH, and the stimulatory effect of cGH could be mediated through SM-C.

Effects of dietary thyroid hormones on growth, plasma T3 and T4, and growth hormone in normal and hypothyroid chickens.

Cockerels and pullets fed with T3 or T4 for 2 weeks showed a decrease in both body weight gain and feed efficiency. The reduction in body weight gain and feed efficiency was dose related in cockerels where T3 or T4 were fed at 0.1, 1.0, and 10.0 ppm levels. T3 and T4 at 0.1 and 1.0 ppm had no significant effects on growth or feed efficiency in pullets, but the 10.0-ppm level of T3 and T4 caused a reduction of -55.24 and -28.18%, respectively, in body weight gain as compared with control birds. T3 was more active than T4 in reducing growth and was toxic when fed at 10.0 ppm both in cockerels and pullets. Both propylthiouracil (PTU)- and methimazole-treated cockerels showed a decrease in rates of gain. T3 and T4 at a dietary level of 0.1 ppm were equipotent in promoting growth in these PTU- and methimazole-treated cockerels, but 10.0 ppm caused a further reduction in body weight gain. Plasma T3 levels were found to be significantly higher in birds that were fed either T3 or T4. Plasma T4 levels were higher in T4-fed birds, but significantly lower in T3-fed birds as compared with controls. Both PTU- and methimazole-treated cockerels had significantly lower plasma T3 and T4 concentrations, but elevated plasma GH concentrations. Dietary T3 and T4 at 1.0 and 10.0 ppm significantly lowered plasma GH concentrations. In summary, these results indicated that T3 was more active than T4 in reducing body weight gain in intact normal birds, but that they were equally potent in promoting growth in PTU- and methimazole-treated hypothyroid birds.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of dietary thyroid hormones on growth and serum T3, T4, and growth hormone in sex-linked dwarf chickens.

Dwarf pullets fed with either T3 or T4 at 0.1, 1.0, and 10.0 ppm for 2 weeks showed no improvement in their body weight gain as compared with birds that were fed a control diet. Birds fed T3 or T4 at 10.0 ppm showed poorer growth, body weight gain, and feed efficiency than control birds. Pullets fed 1.0 ppm of T3 showed significantly better feed efficiency than control birds. Serum T3 concentrations were significantly higher when birds were fed 1.0 ppm of T3 or 10.0 ppm of T3 or T4. Plasma T4 concentrations were also higher in T4 fed birds (1.0 ppm and 10.0 ppm), but were significantly lower in T3 fed birds (1.0 ppm and 10.0 ppm) than in control birds. In birds fed T3 or T4 at 1.0-ppm and 10.0-ppm levels serum growth hormone concentrations were significantly lower as compared with control birds. In conclusion, exogenous T3 and T4 did not correct the sex-linked dwarfism of dwarf chickens. Such dwarfism is characterized by low circulating levels of T3 and T4.

Thyrotropin-releasing hormone stimulates body weight gain and increases thyroid hormones and growth hormone in plasma of cockerels.

The effect of TRH on growth in 4-week-old cockerels was examined in two separate experiments. Daily injection of TRH via the brachial vein stimulated growth in 4-week-old cockerels over 17 days of treatment in the first experiment and over 25 days in the second. In the first experiment, TRH at 1.0 micrograms and 10.0 micrograms/bird caused significant (P less than 0.05) increases of 12.0% and 12.4%, respectively, in growth rate, whereas in the second experiment, only the 1.0 micrograms/bird level of TRH caused an increase (P less than 0.05). In each experiment, the increase in body weight gain was not TRH dose dependent, and neither feed consumption nor feed efficiency was affected. Possible involvement of pituitary hormones in TRH-stimulated growth in cockerels was studied in a separate experiment, and the effects of TRH on plasma T3, T4, and GH were examined. TRH was given iv at 0.1, 1.0, and 10.0 micrograms/bird daily for 5 days, and plasma T3, T4, and GH concentrations were measured 15, 60, and 180 min postinjection by RIA on days 1, 3, and 5. The responses of T3 and T4 to TRH were greatest on day 1, were diminished by days 3 and 5, and were not dose-related. Significant, not dose-related, elevations of plasma GH concentrations were obtained at all doses of TRH. Based on these results, we suggest that TRH has the ability to promote a significant increase in body weight gain in 4-week-old cockerels, and the stimulatory effects may be mediated through GH and/or thyroid hormones.

Antifertility effects of clonidine in laying hens.

Clonidine was anovulatory and markedly antigonadal in laying hens when infused for 1 week from minipump implants at daily rates of 1.08 mg per hen or greater. The ovaries of hens treated with clonidine responded to FSH injections which suggests that the antigonadal effect of clonidine resulted from a reduction in the output of gonadotropin by the pituitary. These data suggest that alpha 2 receptors may be important in regulating avian fertility.

Anticoccidial and tolerance studies in the chicken with two 6-amino-9-(substituted benzyl)purines.

Initial assays of 6-amino-9-(2-chloro-6-fluorobenzyl) purine (MK-302) and 6-amino-9-(2,6-dichlorobenzyl)purine (coded L-628,914) showed potential as anticoccidial agents on the basis of broad-spectrum activity and safety. In battery efficacy studies, dietary levels of 60 to 70 p.p.m. and above MK-302 and 45 to 60 p.p.m. L-628,914 proved to have excellent broad-spectrum anticoccidial activity in chickens given heavy exposure to virulent field isolates of coccidia. Eight-week floor-pen tolerance trials showed that the maximum tolerated diet concentration (MTC) of MK-302 was approximately 95 p.p.m. while the MTC of L-628,914 was approximately 60 p.p.m. Dietary relationships (p.p.m. MK-302:p.p.m. L-628,914 for equivalent effects) derived from the efficacy and tolerance results were 1.2:1 and 1.6:1 respectively and clearly demonstrated a higher therapeutic ratio for MK-302.

Comparison of anticoccidial efficacy, resistance and tolerance of narasin, monensin and lasalocid in chicken battery trials.

The anticoccidial efficacy, host tolerance, and projected resistance development of the three polyether antibiotics, monensin, narasin, and lasalocid were compared. The efficacy of narasin against different coccidial strains was found to parallel that of monensin in as much as strains which were refractory to monensin were also refractory to narasin. In contrast, lasalocid easily controlled some strains which were not well controlled by either narasin or monensin and failed to control one strain readily controlled by these two antibiotics. In growing chicks, lasalocid at the projected use level of 75 p.p.m. and narasin at an efficacious level of 100 p.p.m. were both better tolerated than monensin at the recommended use level of 121 p.p.m. The frequency of mutants resistant to each of these polyether compounds was found to be less than 8.6 X 10(-9) per drug sensitive oocyst for one strain of Eimeria tenella. This corresponds to less than 0.036 and 0.148 as frequent as mutants of this strain resistant to glycarbylamide or to amquinate, respectively.