Growth and carcass characteristics and serum growth hormone, prolactin and insulin profiles in Debouillet lambs treated with ovine growth hormone and(or) zeranol

Sixteen Debouillet wether lambs (approximately 3 mo old) were placed indoors in 1.5- x 3-m pens (14 h light:10 h dark) 28 d after weaning. Lambs received no implant or a 12-mg zeranol implant on d-2 (eight lambs/group). Two days later (d 0), animals received either 0 or 2.5 mg ovine growth hormone (oGH, eight lambs/group) s.c. on alternate days for 42 d. Animals had ad libitum access to water, salt, mineral and a pelleted alfalfa diet (16% CP). After 42 d, lambs were slaughtered to evaluate carcass traits, organ weights and femur characteristics. Zeranol by oGH interactions were not detected (P greater than .20). Zeranol increased (P less than .05) BW, improved (P less than .05) feed:gain during the first 20 d and increased (P less than .10) feed intake during the last 22 d of the 42-d trial compared with controls. Carcass characteristics were not altered (P greater than .10) by 12 mg zeranol. Serum insulin and prolactin were elevated (P less than .05), but serum GH was not influenced by zeranol compared with controls. Exogenous oGH decreased feed intake (P less than .10) and improved feed:gain (P less than .05) during the initial 20 d compared with controls, but did not influence (P greater than .20) these variables during the last 22 d of the study. Carcass traits were not influenced (P greater than .10) by oGH. Exogenous ovine GH dramatically elevated (P less than .05) serum GH, but did not affect serum insulin or prolactin (P greater than .10).(ABSTRACT TRUNCATED AT 250 WORDS)     

The release of growth hormone (GH): relation to the thyrotropic- and corticotropic axis in the chicken

In the chicken and other avian species, the secretion of GH is under a dual stimulatory and inhibitory control of hypothalamic hypophysiotropic factors. Additionally, the thyrotropin-releasing hormone (TRH), contrary to the mammalian situation, is also somatotropic and equally important in releasing GH in chick embryos and juvenile chicks compared to the (mammalian) growth hormone-releasing hormone (GHRH) itself. Consequently, the negative feedback loop for GH release not only involves the insulin-like growth factor IGF-I but also thyroid hormones. In adult chickens, TRH does no longer have a clear thyrotropic activity, whereas its somatotropic activity depends on the feeding status of the animal. In addition, as in mammals, the secretion of GH and glucocorticoids is stimulated by ghrelin, a novel peptide predominantly synthesized in the gastrointestinal tract. Two chicken isoforms of the ghrelin receptor have been identified, both of which are highly expressed in the hypothalamus and pituitary, suggesting that a stimulatory effect may be directed at these levels. GH and glucocorticoids control the peripheral thyroid hormone function by down-regulating the hepatic type III deiodinating enzyme (D3) in embryos (GH and glucocorticoids) and in juvenile and adult chickens (GH). Moreover, glucocorticoids help to regulate T3-homeostasis in the brain during embryogenesis by stimulating the type II deiodinase (D2) expression. This way not only a multifactorial release mechanism exists for GH but also a functional entanglement of activities between the somatotropic-, thyrotropic- and corticotropic axis.     

Luteinizing hormone, follicle stimulating hormone and prolactin secretion in ewes and wethers after zeranol or estradiol injection

Plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) were determined over a 24-h period using radioimmunoassay in sheep injected with corn oil (control) or various doses of zeranol or estradiol-17 beta. Injection of .333, 1 or 10 mg of zeranol caused dose-related increases (P less than .01) in plasma PRL (peak levels at 12 to 18 h) and LH (peak levels at 12 to 20 h) in ovariectomized ewes. Similarly, PRL and LH increased following doses of 33 or 100 microgram of estradiol. Before the LH surge, plasma LH levels were significantly depressed (4 to 8 h). Plasma FSH levels were significantly decreased 4 to 8 h after zeranol and estradiol injection. Slight surges of FSH were observed at times similar to those of LH, but the peak level was never greater than control levels. Injection of 1 mg of zeranol or 100 microgram of estradiol into wethers resulted in a 24-h pattern of PRL secretion not significantly different of LH concentration and significantly prolonged inhibition of FSH secretion. These results indicate similarities in the effects of zeranol and estradiol on anterior pituitary hormone secretion within groups of animals of the same sex or reproductive state. Differences in secretion and plasma concentrations of LH, FSH and PRL due to underlying sexual dimorphism are maintained and expressed even when animals are challenged with structurally different compounds of varying estrogenic potencies.     

Expression of genes for interleukins, neuropeptides, growth hormone receptor, and leptin receptor in adipose tissue from growing broiler chickens

In this study, total RNA was collected from abdominal adipose tissue samples obtained from 10 broiler chickens at 3, 4, 5, and 6 wk of age and prepared for quantitative real-time PCR analysis. Quantitative real-time PCR analysis was used to examine the influence of age on the expression of the adipose tissue genes for IL-1β, -6, -10, -15, -18; brain-derived neurotropic factor; ciliary neurotropic factor; interferon γ, neuropeptide Y receptor Y1; neuropeptide Y; nucleobindin 2; growth hormone receptor; leptin receptor; and visfatin. Between 3 and 6 wk of age, leptin receptor expression decreased (P = 0.013) with age, whereas expression of IL-15 (P = 0.015) and growth hormone receptor (P = 0.002) increased. Furthermore, IL-18 (P < 0.001) and visfatin (P = 0.007) expression increased between 4 and 6 wk of age. This is a unique exhibition of age-related changes in cytokine gene expression in chicken adipose tissue. Future studies are needed to elucidate the role of adipose tissue cytokines in growth and, possibly, disease resistance.     

Influence of zeranol and breed on growth, composition of gain, and plasma hormone concentrations

Seven Angus and six Brangus steers averaging 225 and 245 kg, respectively, were assigned randomly to zeranol (36 mg) implant (I) and no implant (NI) treatments. Steers had ad libitum access to a corn silage diet plus .68 kg of a soybean meal-based supplement fed daily. Steers were bled via jugular catheters on d 0, 28, 56, and 84 at 15-min intervals for 4 h before and 4 h after feeding. Concentrations of growth hormone (GH), insulin (INS), triiodothyronine (T3), thyroxine (T4), and glucose were determined. Whole-body protein and fat contents were monitored. A breed x I interaction (for d 56 to 84 and d 0 to 84) was observed for ADG (P less than .05 and P less than .07, respectively), feed conversion (P less than .05 and P less than .07, respectively), and protein deposition (for d 0 to 29 and d 0 to 84; P less than .07 and P less than .05, respectively). These interactions were attributed to a greater response to I by Angus than by Brangus steers. A feeding x period interaction (P less than .10) was observed for mean GH concentration, and INS, T4, and T3 concentrations were higher (P less than .05) during the 4-h postfeeding period than during the 4-h prefeeding period. The implant increased (P less than .08) mean GH concentration but did not alter the frequency, duration, or amplitude of plasma GH peaks. Steers that were implanted had lower (P less than .05) plasma T3. Brangus steers had lower (P less than .05) plasma glucose, T3, and T4 concentrations than Angus steers. Results indicate that growth factors beyond those measured are responsible for the anabolic response to zeranol.     

Progestin-induced growth hormone (GH) production in the treatment of dogs with congenital GH deficiency

The recent demonstration of the ability of progestins to induce the expression of the growth hormone (GH) gene in the mammary gland of dogs and cats opens possibilities for the treatment of some forms of GH deficiency with progestins. Therefore, one male and one female German shepherd dog with congenital dwarfism because of a pituitary anomaly were treated with subcutaneous injections of medroxyprogesterone acetate (MPA) in doses of 2.5–5.0 mg per kg body weight, initially at 3-wk intervals and subsequently at 6-wk intervals. In both dogs, body sizes increased and a complete adult hair coat developed. Undesirable side-effects were recurrent periods of pruritic pyoderma in both dogs and cystic endometrial hyperplasia with mucometra in the female dog. Parallel with the physical improvements, plasma insulin-like growth factor I concentrations rose sharply. Plasma GH concentrations tended to rise, but never exceeded the upper limit of the reference range. Nevertheless, one of the dogs developed slight acromegalic features, possibly because mammary GH, unlike pituitary GH, is released evenly throughout the day. Even moderate increases in circulating GH concentration may, therefore, give rise to overexposure. It is concluded that long-term treatment with MPA can be used as an alternative for heterologous GH in the treatment of congenital GH deficiency in the dog.     

Inability of heterologous growth hormone (GH) to regulate GH binding protein in GH-transgenic swine

Transgenic pigs expressing bovine, ovine, or human growth hormone (GH) structural genes fused to mouse metallothionein-I (mMT-bGH), ovine MT (oMT-oGH), or mouse transferrin (mTf-hGH) promoters were used to study the effects of GH on the regulation of serum GH-binding protein (GHBP). In the 14 transgenic pigs studied, circulating concentrations of heterologous GH ranged from 15 to 2,750 ng/mL. Using chromatographic methods, specific binding of GH was detected in serum from normal pigs but was undetectable in serum from all the transgenic pigs used, probably as a result of the high serum concentrations of heterologous GH present in these animals. Thus, to avoid interference of binding by high GH concentrations, serum samples were subjected to immunoblotting using a specific anti-GHBP antibody. A specific 54-kDa band was detected in normal pig serum as well as in sera from mMT-bGH, oMT-oGH, and mTf-hGH pigs. Additionally, sera from transgenic mMT-bGH pigs and their sibling controls were subjected to immunoprecipitation with an anti-GHBP antibody followed by immunoblotting with the same antibody. With this technique, we detected two specific bands of 53 and 45 kDa that could represent different degrees of glycosylation of GHBP. As determined by densitometric analysis the amount of GHBP in transgenic pig sera was similar to that detected in sera of the respective control animals. The amount of circulating GHBP remained unchanged even in oMT-oGH and mTf-hGH pigs that were exposed from birth to circulating concentrations of GH as high as 2,750 ng/mL. Thus, we conclude that heterologous GH do not act as modulators ofthe serum GHBP in pigs.     

Changes in plasma non-esterified fatty acids, glucose and alpha-amino nitrogen and their relationship with body weight and plasma growth hormone in growing buffaloes (Bubalus bubalis)

A study was undertaken to investigate the changes of plasma non-esterified fatty acids (NEFA), glucose and alpha-amino nitrogen and their relationship with age, body weight (BW) and plasma growth hormone (GH) in growing buffaloes. For the purpose, six growing female Murrah buffalo calves of 6-8 months of age were selected on the basis of their BW and fed according to Kearl standard (Nutrient Requirements of Ruminants in Developing Countries, International Feedstuffs Institute, Utah State University, Utah, USA, 1982, p. 89) for growing buffaloes (target growth rate 500 g/day) to meet energy and protein requirement of the animals. Blood samples collected at fortnight intervals for 1 year were analysed for plasma NEFA, glucose, alpha-amino nitrogen and GH. The animals were also weighed at fortnight intervals. Plasma NEFA and glucose levels were found to decrease (p < 0.01) with age. Unlike plasma NEFA and glucose, plasma alpha-amino nitrogen level increased (p < 0.01) as the buffaloes become older. Plasma NEFA and glucose concentrations in growing buffaloes were found to be positively correlated with plasma GH (r = 0.379 and 0.420 respectively), but these were non-significant (p > 0.01). However, plasma NEFA and glucose showed a good correlation (p < 0.01; r = 0.780 and 0.652 respectively) with plasma GH per 100 kg live weight. Plasma alpha-amino nitrogen exhibited non-significant (p > 0.01) negative correlation (r = -0.295) with plasma GH but a negative correlation (p < 0.01; r = -0.641) with GH per 100 kg BW. So, plasma metabolites showed a definite pattern of change during growth and these have a significant (p < 0.01) correlation with plasma GH per 100 kg BW than GH.     

Serum concentrations of luteinizing hormone, growth hormone, testosterone, estradiol, and leptin in boars treated with n-methyl-D,L-aspartate

Three experiments were conducted to determine the effects of n-methyl-D,L-aspartate (NMA), an agonist of the excitatory amino acid glutamate, on secretion of hormones in boars. In Exp. 1, boars (185.0+/-.3 d of age; mean +/- SE) received i.v. injections of either 0, 1.25, 2.5, 5, or 10 mg of NMA/kg BW. There were no effects of NMA (P>.1) on secretion of LH and testosterone. Treatment with NMA, however, increased (P<.01) circulating GH concentrations in a dose-dependent manner. In Exp. 2, boars (401 d of age) received an i.v. challenge of NMA at a dose of 10 mg/kg BW or .9% saline. Treatment with NMA, but not saline (P>.1), increased serum concentrations of LH (P<.01), GH (P <.01), and testosterone (P<.06). In Exp. 3, boars that were 152, 221, or 336 d of age were treated i.v. with NMA (10 mg/kg BW). Across ages, treatment with NMA increased circulating concentrations of LH (P<.07) and testosterone (P<.01). However, NMA increased (P<.01) mean GH concentrations in only the oldest boars. Treatment with NMA had no effect (P>.1) on circulating concentrations of estradiol or leptin; however, estradiol concentrations increased (P<.03) with age. In summary, NMA increased secretion of LH, GH, and testosterone in boars. However, endocrine responses to treatment with NMA may be influenced by age of the animal. Finally, NMA did not influence circulating concentrations of estradiol or leptin.     

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.     

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.     

Immunohistochemical detection of growth hormone (GH) in canine hepatoid gland tumors

The aim of this study was to detect immunohistochemically means growth hormone (GH) in 24 hepatoid gland adenomas and 5 hepatoid gland carcinomas and to compare the difference of immunoreactivity between types of tumors. The tumors were classified according to the WHO standards. Tissue sections which were prepared from formalin-fixed, paraffin wax-embedded tissues from 25 male and 4 female dogs were carried out immunostaining using polyclonal primary anti-hGH and EnVision method. Of 24 hepatoid gland adenomas (perianal gland adenomas) 23 (95.8%) were positive. All 5 hepatoid gland carcinomas (perianal gland carcinomas) were positive. No statistically significant differences in percentage of labelled cells between malignant and benign tumors were seen. The present demonstration of GH in hepatoid gland tumors adds new data on GH in extra-pituitary tissues and hormon-dependent tumors.     

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.     

Response to a growth hormone-releasing hormone analog in heifers treated with recombinant growth hormone

Sixteen pregnant Holstein heifers (430kg) were used to determine the effect of long-term administration of a bovine growth hormone (bGH) made by recombinant DNA technology on the ability of a bolus injection of a growth hormone-releasing hormone analog (Ac-His-1, D-Ala-2, Nle-27, GHRH(1-29 NH2) to increase serum GH. Eight heifers received a daily intramuscular injection of bGH (50 mg/day) for 5 months while the other half received a daily injection of physiological saline (control) over the same period. On the last day of bGH treatment and 1, 5, 10 and 25 days after the cessation of bGH treatment, five heifers from each group were challenged with GHRH analog and the response to this releasing hormone analog was measured. Basal GH concentrations were elevated on the last day of treatment in bGH-treated heifers and declined to concentrations similar to control heifers by 1 day after cessation of treatment. Response to GHRH analog was impaired by bGH during the last day of treatment and one day later. Responsiveness returned to a level similar to controls by 5 days after the end of bGH treatment. Response to GHRH analog was lessened during the period of bGH treatment but there were no long term effects on the animals' ability to respond to the releasing hormone.     

黄河裸裂尻生长激素(GH)基因的PCR扩增和克隆

为了克隆黄河裸裂尻生长激素(GH)基因并获得表达产物,试验采用异硫氰酸胍法提取黄河裸裂尻脑组织总RNA,以分离的RNA为模板,采用RT-PCR扩增获得GH基因cDNA,将cDNA插入质粒pQE30中,并在大肠杆菌RB791中表达,经异丙基-β-D-硫代吡喃半乳糖苷(IPTG)诱导后,SDS-PAGE电泳检测蛋白的表达情况。结果表明:扩增后黄河裸裂尻GH基因长度为508 bp,黄河裸裂尻GH基因与青海湖裸鲤的同源性很高,电泳显示出1条新的分子质量约为14.4 ku的特异性条带。     

In vitro effect of leptin on growth hormone (GH)- and insulin-like growth factor-I (IGF-I)-stimulated progesterone secretion and apoptosis in developing and mature corpora lutea of pig ovaries

This study was designed to determine whether leptin modulates growth hormone (GH)- and insulin like growth factor-I (IGF-I)-stimulated progesterone (P4) production by corpora lutea (CL). Luteal cells were recovered from early developing (ELP) and mature (MLP) corpora lutea and cultured in defined medium with various combinations of GH, IGF-I, and leptin (0-200 ng/ml). P4 concentrations in the media were determined after 48 h of culture. During the early luteal phase, leptin at all used doses had no effect on basal P4 secretion, but it did suppress caspase-3 activity. When added in combination with GH, it had no effect on either GH-stimulated P4 secretion or apoptosis. Concomitant treatment with IGF-I and leptin decreased P4 secretion and parallelly increased the apoptosis rate. In mature corpora lutea of full secreting capacity, leptin at all doses had no effect on basal and GH-stimulated P4 secretion and caspase-3 activity. Only at the highest dose (200 ng/ml) when leptin was added with IGF-I did P4 secretion decrease with no effect on the caspase-3 activity. We conclude that the role of leptin is to restrict the stage of CL formation. During this luteal phase, leptin acts as an antiapoptotic factor and, at the same time, reverses antiapoptotic action of IGF-I, thereby protecting cells from excessive apoptosis and supporting retention of appropriate cell numbers, which is necessary for maintenance of homeostasis in developing CL.     

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.