Effect of dose and route of administration of thyroid releasing hormone (TRH) on the concentration of prolactin (PRL) and thyroxine (T4) in cyclic gilts

Our objective was to examine the ability of thyroid releasing hormone (TRH) to stimulate not only the release of the thyroid hormones, but also prolactin (PRL) in the female pig. An experiment was conducted to determine the effect of dose and route of administration of TRH on the concentration of PRL and thyroxine (T4) in cyclic gilts. Six gilts were injected with 0, 5, 25, 125, and 625 micrograms TRH and fed 0, 5, 2.5, 12.5 and 62.5 mg TRH. Gilts received TRH once daily. During the 10-day treatment period, route of TRH administration alternated between i.v. injection and feeding. The dose of TRH progressed from the lowest to the highest. Blood samples were taken prior to TRH injection and thereafter at 15-min intervals for 3 hr. Sampling continued for an additional 3 hr at 30-min intervals when TRH was fed. Concentrations of PRL and T4 were determined by radioimmunoassay. Intravenous injection of gilts with 125 and 625 micrograms TRH resulted in an increase in PRL from 0 to 15 min (P less than .05). All doses of TRH given i.v. elevated T4 over a 2-hr period (P less than .01). TRH failed to increase PRL when TRH was fed (P greater than .5). The feeding of 62.5 mg TRH elevated T4 from 0 to 6 hr (P less than .01). Thus, TRH injection increased PRL rapidly and T4 gradually. When TRH was fed, only a gradual elevation in T4 was observed. We conclude that TRH can elicit the release of both PRL and T4 in the cyclic gilt, but magnitude and duration of the PRL and T4 response depends on the dose and route of TRH administration.     

Peripheral T lymphocyte changes in neonatal piglets: Relationship with growth hormone (GH), prolactin (PRL) and cortisol changes

Taking into account the role played by the neuroendocrine network in affecting the early development of the immune response, the present study aims to assess neonatal immunity in piglets by testing peripheral lymphocyte age-related changes in relationship to plasma levels of some relevant immunoregulatory hormones, such as growth hormone (GH), prolactin (PRL) and cortisol. For this purpose, we studied the peripheral lymphocyte age-related changes in relationship to plasma levels of GH, PRL and cortisol in conventional piglets from birth (day 0) to 41 days of age. A significant decrease was observed in the total number of lymphocytes at day 0, with a subsequent constant increment up to 41 days of age. Concomitantly, the number of T cell subsets (mainly CD8(+) cells and double positive CD4(+)CD8(+)) was low at birth, with strong increments between the 19th and 41st days of life. The CD4(+) T cell number subset was less diminished at birth than that of CD8(+), albeit with significant increments in the post-weaning period. Of interest, gammadelta T cells, which are more involved in innate immune efficiency, displayed the same trend as CD8(+) T cells from birth to the 41st day of life. From day 0 up to the 19th day, significant inverse correlations were found between T cell subsets and GH or PRL or cortisol, albeit with more significant inverse correlations with cortisol. The high levels of GH and PRL in the pre-weaning period may be due to the fact that they have to counteract the cortisol-mediated negative effect on lymphocyte production and development. These findings suggest that stress condition occurs at birth with decreases in the immune parameters, in the same way as in human newborns, with a subsequent gradual normalisation and immune development, as shown by decreased cortisol, GH and PRL normalisation and concomitant increments in T cell subsets.     

Effect of long-term administration of porcine growth hormone-releasing factor and(or) thyrotropin-releasing factor on growth hormone, prolactin and thyroxine concentrations in growing pigs

Long-term administration of porcine growth hormone-releasing factor (pGRF(1-29)NH2) and(or) thyrotropin-releasing factor (TRF) was evaluated on serum concentrations of growth hormone (GH) thyroxine (T4) and prolactin (PRL). Twenty-four 12-wk-old female Yorkshire-Landrace pigs were injected at 1000 and 1600 for 12 wk with either saline, pGRF (15 micrograms/kg), TRF (6 micrograms/kg) or pGRF + TRF using a 2 x 2 factorial design. Blood samples were collected on d 1, 29, 57 and 85 of treatment from 0400 to 2200. Areas under the GH, T4 and PRL curves (AUC) for the 6 h (0400 to 1000) prior to injection were subtracted from the postinjection periods (1000 to 1600, 1600 to 2200) to calculate the net hormonal response. The AUC of GH for the first 6 h decreased similarly (P less than .05) with age for all treatments. The GH response to GRF remained unchanged (P greater than .10) across age. TRF alone did not stimulate (P less than .05) GH release but acted in synergy with GRF to increase (P less than .05) GH release. TRF stimulated (P less than .001) the net response of T4 on all sampling days. Animals treated with the combination of GRF + TRF showed a decreased T4 AUC during the first 6 h on the last three sampling days. Basal PRL decreased (P less than .05) with age. Over the four sampling days, animals injected with TRF alone showed (P less than .01) a reduction (linear effect; P less than .01) followed by an increase (quadratic effect; P less than .05) in total PRL concentration after injection; however, when GRF was combined with TRF, such effects were not observed (P greater than .10). Results showed that 1) chronic injections of GRF for 12 wk sustained GH concentration, 2) TRF and GRF acted synergistically to elevate GH AUC, 3) TRF increased T4 concentrations throughout the 12-wk treatment period, 4) chronic TRF treatment decreased the basal PRL concentration and 5) chronic GRF + TRF treatment decreased the basal concentration of T4.     

Measurement of thyroid hormones (thyroxine, T4; triiodothyronine, T3) in captive nondomestic felids.

The aim of this research was to obtain basic values for the evaluation of thyroid function in nondomestic felids. Serum thyroid hormone concentrations (thyroxine, T4; triiodothyronine, T3) were measured by radioimmunoassay in 145 cats, representing nine species of captive nondomestic felids: jaguar (Panthera onca), n = 49; puma (Puma concolor), n = 10; ocelot (Leopardus pardalis), n = 22; oncilla (Leopardus tigrinus), n = 12; geoffroy (Oncifelis geoffroyi), n = 4; jaguarundi (Herpailurus yaguarondi), n = 8; margay (Leopardus wiedii), n = 7; lion (Panthera leo), n = 26; and tiger (Panthera tigris), n = 7. For each species, mean +/- SEM of T3 and T4, respectively, were as follows: jaguar, 0.56 +/- 0.03 and 9.7 +/- 0.8 ng/ml; puma, 0.67 +/- 0.04 and 11.2 +/- 1.2 ng/ml; ocelot, 0.48 +/- 0.03 and 13.8 +/- 1.5 ng/ml; oncilla, 0.43 +/- 0.03 and 10.0 +/- 1.6 ng/ml; geoffroy, 0.44 +/- 0.04 and 8.0 +/- 0.16 ng/ml; jaguarundi, 0.7 +/- 0.03 and 5.0 +/- 1.0 ng/ml; margay, 0.48 +/- 0.04 and 12.2 +/- 2.3 ng/ml; lion, 0.43 +/- 0.02 and 5.7 +/- 2.6 ng/ml; and tiger, 0.66 +/- 0.03 and 12.6 +/- 0.9 ng/ml. Within species, T3 and T4 concentrations did not differ (P > 0.05) between males and females.     

Serum thyroxine (T4) and triiodothyronine (T3) uptake values in normal adult cats as determined by radioimmunoassay

Radioimmunoassay procedures employing highly specific antibodies for either serum T4 or T3 were utilized to determine T4 concentrations and T3 uptake values in normal cats. Mean values for serum T4 and for T3 uptake were 30.9 ng/ml +/- 19 ng/ml and 59.67% +/- 12.2%, respectively.     

Effects of dietary phytoestrogens on plasma testosterone and triiodothyronine (T3) levels in male goat kids

Background

Exposure to xenoestrogens in humans and animals has gained increasing attention due to the effects of these compounds on reproduction. The present study was undertaken to investigate the influence of low-dose dietary phytoestrogen exposure, i.e. a mixture of genistein, daidzein, biochanin A and formononetin, on the establishment of testosterone production during puberty in male goat kids.

Methods

Goat kids at the age of 3 months received either a standard diet or a diet supplemented with phytoestrogens (3 - 4 mg/kg/day) for ~3 months. Plasma testosterone and total and free triiodothyronine (T₃) concentrations were determined weekly. Testicular levels of testosterone and cAMP were measured at the end of the experiment. Repeated measurement analysis of variance using the MIXED procedure on the generated averages, according to the Statistical Analysis System program package (Release 6.12, 1996, SAS Institute Inc., Cary, NC, USA) was carried out.

Results

No significant difference in plasma testosterone concentration between the groups was detected during the first 7 weeks. However, at the age of 5 months (i.e. October 1, week 8) phytoestrogen-treated animals showed significantly higher testosterone concentrations than control animals (37.5 nmol/l vs 19.1 nmol/l). This elevation was preceded by a rise in plasma total T₃ that occurred on September 17 (week 6). A slightly higher concentration of free T₃ was detected in the phytoestrogen group at the same time point, but it was not until October 8 and 15 (week 9 and 10) that a significant difference was found between the groups. At the termination of the experiment, testicular cAMP levels were significantly lower in goats fed a phytoestrogen-supplemented diet. Phytoestrogen-fed animals also had lower plasma and testicular testosterone concentrations, but these differences were not statistically significant.

Conclusion

Our findings suggest that phytoestrogens can stimulate testosterone synthesis during puberty in male goats by increasing the secretion of T₃; a hormone known to stimulate Leydig cell steroidogenesis. It is possible that feedback signalling underlies the tendency towards decreased steroid production at the end of the experiment.     

Oral administration of peptidergic growth hormone (GH) secretagogue KP102 stimulates GH release in goats

To assess the oral activity of KP102 (also known GHRP-2) on growth hormone (GH) release in ruminant animals, 5 or 10 mg/kg body weight (BW) of KP102 dissolved in saline was orally administered twice at 2 hr-intervals to either 1- or 3-mo-old goats (n = 5-6). Plasma GH concentrations in the 1-mo-old goats were elevated at 15 min after the first administration of both 5 and 10 mg/kg BW of KP102. Significant elevation of GH concentrations continued until 180 min after 10 mg/kg BW of KP102, whereas the elevated GH levels after the administrations of 5 mg/kg BW of KP102 subsided to basal concentrations within 90 min. The second administration of 10 mg/kg BW of KP102 failed to elevate the GH concentration, but 5 mg/kg BW of KP102 abruptly stimulated GH release. Plasma GH concentrations in the 3-mo-old goats were also significantly elevated after the administration of both 5 and 10 mg/kg BW of KP102. The plasma GH responses to 5 and 10 mg/kg BW of KP102 were almost identical. The elevated GH levels after the first administration of KP102 tended to be maintained throughout the experiment, and a transient increase in plasma GH levels was observed after the second administration. However, the stimulatory effect of KP102 on GH release in the 3-mo-old goats was small and less abrupt than that in the 1-mo-old goats. The concentrations of insulin-like growth factor-I were not increased by KP102 during the brief sampling periods used in this experiment. These results show that the oral administration of the peptidergic GH secretogogue KP102 stimulates GH release in a ruminant species, and that the oral activity of KP102 on GH release is modified by the age.     

Effect of triglycerides on growth hormone (GH)-releasing factor-mediated GH secretion in newborn calves

The effect of triglycerides (Tg) on GRF-mediated GH secretion was examined in 2 groups of twelve ten-day old male calves. Twelve calves were intravenously infused with a lipid-heparin solution (5 mg Tg and 0.3 IU heparin/kg body wt/min for 90 min). The twelve control calves received in the same way, the same volume of saline. Thirty minutes after the start of infusion, GRF 1–29 (human amide, 0.16 μg/kg body wt) was intravenously injected in six animals of each group.

Mean plasma GH levels reached peak concentrations in the 2 groups 5 min after GRF injection. However the area under the GH response curve, when lipid-heparin was given, was significantly diminished compared to the response when saline was given. In the same time, lipid-heparin treatment increased plasma SRIF concentration. These data suggest that an increase in plasma Tg concentration, induced by lipid-heparin infusion, inhibits GRF-mediated GH secretion, possibly through stimulation of SRIF secretion.     

Effect of long-term administration of human growth hormone-releasing factor and (or) thyrotropin-releasing factor on hormone concentrations in lactating dairy cows

Fifteen cows (87 +/- 8 d in lactation; 641 +/- 33 kg BW) were randomly assigned to treatment and then subjected for 182 d to daily sc injection (1000 hr), in the cervical area, of saline (control), thyrotropin-releasing factor (TRF: 1 micrograms/kg BW), growth hormone-releasing factor (1-29)NH2 (GRF; 10 micrograms/kg BW) or GRF plus TRF (10 and 1 micrograms/kg BW, respectively) according to a 2 x 2 factorial design. On days 1, 31, 88 and 179, jugular blood samples were collected from 2 hr before to 6 hr after injection. Samples were also collected for 5 consecutive days after cessation of treatment. GRF always induced growth hormone (GH) release (600 vs 7925 ng.min/ml) with augmentation of response with time (interaction GRF * day; P less than .001). TRF did not affect (P greater than .25) GH release; there was no interaction (P greater than .25) with time. There was no significant interaction (P greater than .25) between GRF and TRF on GH release. However, the amount of GH release with GRF plus TRF was always greater than with GRF alone (9419 vs 6431 ng.min/ml). TRF induced a significant release of prolactin (23769 vs 42175 ng.min/ml) but GRF reduced the amount of prolactin release on the last day of sampling. TRF induced thyroid stimulating hormone (TSH) release only on the first day of injection while triiodothyronine (T3) and thyroxine (T4) continued to respond to TRF throughout the treatment period. Concentrations of T3 and T4 fell below control levels after cessation of TRF injection. In conclusion, GRF-induced GH release and TRF-induced Prl and thyroid hormone release were maintained over a 6-mo treatment period. TRF induced TSH release only on the first day of injection. Overall, these results raised the possibility of a direct effect of TRF on the thyroid gland.     

Effect of thyrotropin releasing hormone (TRH) on serum levels of thyroid hormones in thoroughbred mares

Effects of thyrotropin releasing hormone (TRH) on serum levels of thyroid hormones were studied in 12 Thoroughbred mares. Significant increases (P<0.05) of serum T4 levels occurred as early as 2 hours and peaked at 4–10 hours after intravenous injection of 0.5 – 5 mg TRH. Following injection of 0.5, 1, 3 and 5 mg of TRH the serum levels of T4 were increased 2.25, 2.42,2.42 and 3.67 fold, respectively, over pre-injection levels. Serum levels of T3 were also significantly increased (P<0.05) at 1 or 2 hours and peaked at 2 to 4 hoursafter injection. The mean peak increase of T₃ levels were 2.87, 3.21, 3.10 and 3.10 fold over pre- injected in level in 0.5, 1, 3,5 mg treated horses, respectively. These results suggest that TRH can be an alternative to heterologous TSH for the equine thyroid function test. The recommended dosage is 1–3 mg, and most appropriate time to collect post-TRH blood sample is between 4–6 hours. Serum levels of T₄ and T₃ should increase 2–3 fold from baseline in normal horses.     

Effect of propranolol on growth hormone response to GH releasing hormone (GHRH 1-44) in the dog.

The present study was undertaken to examine whether beta-adrenergic blockade with propranolol might influence and make less variable the growth hormone (GH) response to exogenous GH releasing hormone (GHRH) 1-44 in the dog. On four separate occasions eight healthy beagles, one to two years old, randomly received either propranolol (40 micrograms kg-1 intravenously) or an equivalent volume of saline, 30 minutes before either GHRH 1-44 (1 microgram kg-1 intravenously) or vehicle was injected. After propranolol alone, GH secretion did not differ from saline (area under the curve [AUC]: 649.5 +/- 128.3 v 633.2 +/- 87.7 ng min ml-1, respectively). GHRH alone elicited a significant increase in GH secretion (AUC: 1230.5 +/- 210.5 ng min ml-1) with a peak concentration of 16.7 +/- 4.8 ng ml-1. When GHRH was injected after propranolol the mean peak (59.1 +/- 14.7 ng ml-1) and secretory area (AUC: 2631.0 +/- 474.4 ng min ml-1) were greater than those observed after GHRH alone. However, from a clinical point of view propranolol pretreatment does not modify the great individual variability of the GH response to GHRH.     

Interaction between salsolinol (SAL) and thyrotropin-releasing hormone (TRH) or dopamine (DA) on the secretion of prolactin in ruminants

We have recently demonstrated that salsolinol (SAL), a dopamine (DA)-derived compound, is present in the posterior pituitary gland and is able to stimulate the release of prolactin (PRL) in ruminants. The aim of the present study was to clarify the effect that the interaction of SAL with thyrotropin-releasing hormone (TRH) or DA has on the secretion of PRL in ruminants. A single intravenous (i.v.) injection of SAL (5mg/kg body weight (b.w.)), TRH (1microg/kg b.w.), and SAL plus TRH significantly stimulated the release of PRL in goats (P<0.05). The cumulative response curve (area under the curve: AUC) during 120min was 1.53 and 1.47 times greater after the injection of SAL plus TRH than either SAL or TRH alone, respectively (P<0.05). A single i.v. injection of sulpiride (a DA receptor antagonist, 0.1mg/kg b.w.), sulpiride plus SAL (5mg/kg b.w.), and sulpiride plus TRH (1microg/kg b.w.) significantly stimulated the release of PRL in goats (P<0.05). The AUC of PRL during 120min was 2.12 and 1.78 times greater after the injection of sulpiride plus TRH than either sulpiride alone or sulpiride plus SAL, respectively (P<0.05). In cultured bovine anterior pituitary (AP) cells, SAL (10(-6)M), TRH (10(-8)M), and SAL plus TRH significantly increased the release of PRL (P<0.05), but the additive effect of SAL and TRH detected in vivo was not observed in vitro. In contrast, DA (10(-6)M) inhibited the TRH-, as well as SAL-induced PRL release in vitro. All together, these results clearly show that SAL can stimulate the release of PRL in ruminants. Furthermore, they also demonstrate that the additive effect of SAL and TRH on the release of PRL detected in vivo may not be mediated at the level of the AP, but that DA can overcome their releasing activity both in vivo and in vitro, confirming the dominant role of DA in the inhibitory regulation of PRL secretion in ruminants.     

Effect of frequency of administration of exogenous porcine growth hormone on growth and carcass traits and ovarian function of prepubertal gilts.

Three experiments were conducted to examine relationships among dose and frequency of administration of exogenous porcine growth hormone (pGH) on growth traits and ovarian function of prepubertal gilts. In Exp. 1, gilts were treated with 0 or 5 mg of pGH daily for 42 d or 5 mg of pGH daily on alternate weeks over a 42-d period. In Exp. 2, gilts were treated with 0, 2.5, or 5 mg of pGH daily for 31 d or daily on alternate weeks for 31 d. In Exp. 3, gilts received 5 mg of pGH daily on either wk 1, 3, and 5 or wk 2, 4, and 6 during a 42-d period. In all experiments, ADG increased dramatically and feed efficiency improved markedly during treatment with pGH, and both traits declined rapidly during periods when treatment was withdrawn. Gilts treated with pGH daily on alternate weeks tended to be more similar (P greater than .05) to control gilts for growth rate, feed efficiency, and carcass measurements than to gilts that received continuous daily administration of pGH during the entire duration of the experiments. Increased concentrations of estradiol and insulin-like growth factor (IGF)-I in follicular fluid and serum, decreased concentrations of IGF-II in follicular fluid, and increased weights of ovaries were evident as both dose and frequency of exogenous pGH administration increased. Therefore, gilts are extremely sensitive to administration and withdrawal of exogenous pGH during the finishing phase of the production cycle and can respond within 7 d to changes in exogenous pGH treatment regimens. Alternate weekly administration of exogenous pGH in vivo may improve follicular function, as indicated by relationships among IGF-I and IGF-II, estradiol, and progesterone, but fails to improve overall growth and carcass traits compared with controls.     

Effect of human growth hormone-releasing factor and(or) thyrotropin-releasing factor on hormone concentrations in dairy calves

To determine the effect of chronic treatment with human growth hormone-releasing factor (1-29)NH2 (GRF) and(or) thyrotropin-releasing factor (TRF), 20 calves averaging 70.2 kg BW were divided into four groups (n = 5) according to a 2 X 2 factorial design. For 86 d, calves in each group received twice daily s.c. injections of either .9% NaCl, GRF (5 micrograms/kg BW), TRF (1 microgram/kg BW) or GRF (5 micrograms/kg BW) plus TRF (1 microgram/kg BW). On d 87, all calves received a s.c. injection of GRF (5 micrograms/kg BW) plus TRF (1 microgram/kg BW). Blood samples were collected every 20 min for 18 h on d 1, 29, 57 and 85, and for 8 h on d 87. Hormone responses were measured as area under the hormone concentration curve over time. GRF and TRF acted in synergy (P less than .10) on GH release throughout the treatment period. Growth hormone responsiveness to GRF and(or) TRF decreased (P less than .01) with days of treatment, but this decrease was due to aging rather than to chronic treatment, because GH response to GRF plus TRF was similar (P greater than .10) between control and treated calves on d 87. TRF increased prolactin (Prl) concentration until the end of the treatment period (P less than .01). The response of thyroid-stimulating hormone (TSH) to TRF disappeared (P greater than .10) after 1 mo of treatment, whereas the thyroxine (T4) response decreased (P less than .01) throughout the treatment period. GRF did not induce nor did it interact with TRF on TSH and T4 release.(ABSTRACT TRUNCATED AT 250 WORDS)     

5种品系肉用仔鸡血清IGF-Ⅰ和甲状腺激素与生产性能相关性研究

为了对肉鸡选种选育提供科学依据,本研究选择5个不同生长速度的肉鸡品系,相同饲养条件下饲养8周,记录饲料消耗及生长速度,于第8周末宰杀,采集血清,放免测定法测定其中的IGF-Ⅰ、T3和T4浓度。结果表明生长最慢的烟霞鸡具有显著高水平的T3和显著低水平的IGF-Ⅰ以及显著低的全净膛率。动物的生长速度与血清IGF-Ⅰ水平呈现显著正相关,与血清T3水平呈现显著负相关。血清IGF-Ⅰ与T3水平呈现显著负相关。全净膛率与血清IGF-Ⅰ及T4水平呈显著正相关。肉鸡生长速度与血清IGF-Ⅰ及T3水平有密切关系,禽类生长发育的调节机制显著不同于哺乳类。     

Effect of constant versus adjusted dose of exogenous porcine growth hormone (pGH) on growth and reproductive characteristics of gilts

Growth, carcass traits, and selected reproductive characteristics were evaluated in prepubertal gilts treated with either a constant mass of pGH or a mass of pGH adjusted periodically for changes in BW. Gilts (64 kg, n = 24) were given 24 daily injections of either vehicle (C; control) or one of two doses of pGH: 70 micrograms/kg of BW, with dose adjusted every 5th d for changes in BW (A; adjusted), or 70 micrograms/kg of initial BW (U; unadjusted). Gilts were slaughtered on d 25. Gilts treated with pGH had higher ADG (P less than .002) and improved feed efficiency (kg of feed/kg of gain; P = .0003) compared with controls. Weights of adrenal glands, liver, heart, and kidney were higher (all P less than .01) for Groups A and U than for Group C gilts. Average backfat thickness was less (P less than .004) for A and U gilts than for C gilts and less for Group A than for Group U (P less than .02). Furthermore, growth and carcass traits were similar (P greater than .05) for Groups A and U, except for measurements of first rib backfat, last rib backfat, and average backfat depth (P less than .05). Culture of granulosa cells (GC) was employed to assess ovarian function. Addition of FSH to the culture media enhanced secretion of progesterone (P4) by cultured GC from all in vivo treatments compared with unsupplemented cultures of GC (P less than .05). Addition of LH to the culture media enhanced secretion of P4 by cultured GC from pGH-treated gilts only (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

New insights into the mechanism and actions of growth hormone (GH) in poultry.

Despite well documented anabolic effects of GH in mammals, a clear demonstration of such responses in domestic poultry is lacking. Recently, comprehensive dose-response studies of GH have been conducted in broilers during late post-hatch development (8 to 9 weeks of age). GH reduced feed intake (FI) and body weight gain in a dose-dependent manner, whereas birds pair-fed to the level of voluntary FI of GH-infused birds did not differ from controls. The reduction in voluntary FI may involve centrally mediated mechanisms, as hypothalamic neuropeptide Y protein and mRNA were reduced with GH, coincident with the maximal depression in FI. Growth of breast muscle was also reduced in a dose-dependent manner. Circulating IGF-I was not enhanced by GH, despite evidence that early events in the GH signaling pathway were intact. A GH dose-dependent increase in circulating 3,3',5-triiodothyronine(T3) paralleled decreases in hepatic 5D-III monodeiodinase activity, whereas 5'D-I activity was not altered. This confirms that a marked hyperthyroid response to GH occurs in late posthatch chickens, resulting from a decrease in the degradative pathway of T3 metabolism. This secondary hyperthyroidism would account for the decreased skeletal muscle mass (52) and lack of enhanced IGF-I (53) in GH-treated birds. Based upon these studies, it is now evident that GH does in fact have significant effects in poultry, but metabolic responses may confound the anabolic potential of the hormone.     

Neuroendocrine regulation of growth hormone secretion in sheep. II. Effect of somatostatin on growth hormone and glucose levels.

The effect of intravenous (iv) and intracerebroventricular (icv) administration of somatostatin on the plasma levels of growth hormone (GH) and glucose was studied in sheep. Intravenous somatostatin decreased (P less than 0.001) circulating GH when infused at the rate of 5 micrograms/min (150 ng/kg/min) over 1 hr, but when used at 1 microgram/min there was no effect on plasma GH levels during infusion. At both doses used there was an indication of an increase in GH following the cessation of somatostatin infusion. Somatostatin given at both these doses iv had no effect on plasma glucose levels. When given icv neither 1.8 micrograms, 18 micrograms nor 180 micrograms somatostatin had any significant effect of plasma GH levels, although there was a significant (P less than 0.05) elevation in GH levels 75 min after 180 micrograms somatostatin icv. Plasma glucose levels did not increase following injection of somatostatin icv at 1.8 or 18 micrograms, but there was a clear hyperglycaemic episode following 180 micrograms icv. Despite a lack of effect of somatostatin on GH release when given icv, there was a clear elevation (P less than 0.05) in plasma GH levels immediately following icv administration of a somatostatin antiserum. These data indicate that iv administration of somatostatin at pharmacological levels can depress unstimulated GH levels in sheep while administration icv does not. Central administration of somatostatin increases plasma glucose levels only at high doses and seems unlikely to be of physiological importance in glucose homeostasis.