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ABSTRACT
The possible role of thyroid hormones in the rise in plasma GH observed in protein-restricted chicks was examined. Increased sensitivity of protein-restricted chicks to secretagogue challenge (TRH or GH-releasing factor) appears to account, at least in part, for increased GH concentrations in protein-restricted chicks. Thyroid hormones administered acutely were able to suppress plasma GH concentrations in protein-restricted chicks. Further, chronic thyroid hormone supplementation to low protein diets normalized circulating thyroid hormone concentrations and also normalized the response to GH secretagogue challenge. This decreased sensitivity to TRH provocation occurred without an accompanying change in plasma concentrations of insulin-like growth factor-I, a reputed inhibitor of GH secretion in the chicken.
J. Endocr. (1988) 117, 223–228
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The rate of disappearance of luteinizing hormone (LH) from the circulation is an important parameter in studying the dynamics of the hormone and in interpreting the significance of both circulating and pituitary hormonal levels. This rate is most frequently expressed in terms of the half-life of LH in the circulation (see Parlow, 1968). The estimation of the half-life of circulating LH in birds has been made feasible by the availability of purified chicken gonadotrophins (Stockell Hartree & Cunningham, 1969; Scanes & Follett, 1972), together with a radioimmunoassay for avian LH (Follett, Scanes & Cunningham, 1972).
The half-life of LH in the domestic fowl was determined by following the dis-appearance of either unlabelled LH or 125I-labelled LH from the circulation of the bird. In the case of the labelled hormone, a chicken LH fraction of high ovarian ascorbic acid depleting activity and low thyrotrophin content (fraction AEI, Scanes & Follett,
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Introduction
Somatostatin (SRIF) and growth hormone-releasing factor (GRF) are well characterized as hypothalamic neuropeptides which, respectively, inhibit and stimulate the secretion of growth hormone (GH). SRIF is also produced by pancreatic D cells and cells within the gut, where it can act to regulate pancreatic and gastrointestinal hormone secretion. A number of laboratories have demonstrated that the synthesis, receptors and endocrine activities of GRF and SRIF may be influenced by immune factors, such as the cytokines interleukin-1 (IL-1) (Scarborough et al. 1989, Lumpkin 1990, Campbell et al. 1991b, Honegger et al. 1991, Payne et al. 1992, Peisen et al. 1992, 1994), IL-2 (Karanth et al. 1992), IL-6 (Spangelo et al. 1989) and tumor necrosis factor-α (TNF-α) (Scarborough & Dinarello 1989, Walton & Cronin 1989, Gaillard et al. 1990, Elsasser et al. 1991) as well as lipopolysaccharide endotoxin (LPS), an inducer of cytokines (Kasting & Martin 1982, Yelich et al. 1993).
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SUMMARY
Chicken growth hormone has been isolated from adenohypophysial tissue from which the glycoprotein hormones had been removed. The procedure entailed alkali extraction, ammonium sulphate precipitation and ion-exchange chromatography on DEAE-cellulose. The resulting fraction was homogeneous, active in the rat tibia bioassay and had a similar isoelectric point, molecular weight and amino acid composition to mammalian growth hormone. A specific homologous radioimmunoassay has been developed using the avian growth hormone.
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The effect of prostaglandin (PG) E1, PGE2 and PGF2α on GH secretion has been assessed in immature domestic fowl. The intravenous or subcutaneous administration of PGE1 and PGE2 (at a dose of approximately 200 μg/kg) to 2-, 6- and 8-week-old cockerels consistently lowered plasma GH concentrations. This inhibition in GH secretion was observed for at least 40 min after administration of PGE1 and PGE2. The same dose of PGF2α suppressed plasma GH levels in 2- and 6-week-old birds but the magnitude and duration of this response was less than that induced by PGE1 and PGE2. At this dose, administration of PGE1 and PGE2 resulted in overt signs of distress (e.g. gaping, panting, eye closure and postural instability) within 5–10 min of injection and the birds appeared to be sedated thereafter. Prostaglandin F2α and lower doses of PGE1 and PGE2 did not have any apparent effect on behaviour. These results suggest that prostaglandins inhibit GH secretion in birds although this may reflect a non-specific stress response.
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Department of Zoology, University of Hull, Hull, HU6 7RX and * Department of Physiology, Rutgers University, New Brunswick, New Jersey 08903, U.S.A.
(Received 9 May 1978)
Recent avian studies (Harvey, Godden & Scanes, 1977; Harvey, Scanes, Falconer, Bolton & Chadwick, 1977) have established a definite pattern of growth hormone (GH) secretion during growth, with high plasma concentrations in young growing birds and low levels in adults. These observations indicate that the concentration of immunoreactive GH in the circulation may be related to the rate of body growth. The aim of the present study was, therefore, to determine whether experimental modification of growth was accompanied by corresponding alterations in GH secretion. Since testosterone suppresses growth in cockerels (Visco, 1973), plasma concentrations of GH were determined during growth in control and testosterone-implanted birds.
Seven 2-week-old cockerels (Thornber 909 strain) were implanted subcutaneously with a testosterone pellet (Intervet, 100 mg) in the nape
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ABSTRACT
Surgical thyroidectomy increases basal and TRH-induced GH concentrations in the peripheral plasma of immature domestic fowl. Replacement therapy with thyroxine (T4; 100 μg/kg per day for 7 days, i.m.) suppressed the GH responses to thyroidectomy. Bolus administration of T4 (10 μg/kg, i.m.) to thyroidectomized birds promptly lowered the circulating GH concentrations, which remained suppressed for at least 4 h. Chronic (daily injections for 7 days) or acute (one injection) pretreatment of thyroidectomized birds with iopanoic acid (IOP; 40 mg/bird, i.m.) before the bolus administration of T4 attenuated, but did not prevent, inhibition of circulating GH levels by T4. Administration of IOP (40 mg/bird i.m.) 24 h and immediately before the administration of tri-iodothyronine (T3; 3 μg/kg, i.m.) or T4 (10 μg/kg, i.m.) also failed to suppress thyroidal inhibition of circulating GH concentrations in thyroidectomized birds. Administration of IOP alone had no effect on GH concentrations. Circulating T3 concentrations were not enhanced following the administration of T4 to IOP-treated birds, indicating its inhibition of hepatic monodeiodinase activity.
The metabolic clearance rate (MCR) of 125I-labelled chicken GH in the plasma of thyroidectomized fowl was less than that in sham-thyroidectomized birds. Following pretreatment with T4 (100 μg/kg per day for 7 days) sham-thyroidectomized and thyroidectomized birds did not differ significantly in their MCR. The GH secretion rate in thyroidectomized birds was similar to that in sham-thyroidectomized birds and in both groups was markedly reduced following pretreatment with T4.
These results demonstrate thyroidal inhibition of circulating GH concentrations in fowl. Both T3 and T4 inhibited GH concentrations and the effect of T4 was not simply due to its role as a T3 prohormone. In the absence of thyroid hormones, the MCR of GH was reduced but its secretion rate was not enhanced. A significant reduction of GH secretion rate occurs in response to exogenous T4, in the absence of any change in GH metabolism.
Journal of Endocrinology (1990) 124, 215–223
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Plasma levels of GH and prolactin were measured by radioimmunoassay in male domestic fowl treated with centrally active agents. p-Chlorophenylalanine (pCPA) did not have an effect on tonic levels of prolactin but led to a significant rise in circulating GH concentrations. The three serotonin receptor antagonists tested, methysergide, SQ-10631 and cyproheptadine, each resulted in a significant reduction in plasma prolactin while markedly increasing plasma GH levels. Administration of 5-hydroxytryptophan led to a rise in plasma prolactin and a drop in plasma GH levels in untreated birds or in animals pretreated with pCPA. The serotonin receptor agonist, quipazine, resulted in a marked increase in plasma prolactin and a marked reduction in plasma GH concentrations in untreated birds. In pCPA-pretreated animals quipazine was no longer effective in altering plasma prolactin levels but still caused a significant drop in circulating levels of GH. These results suggest that in the young male domestic fowl serotonin has a stimulatory role in the regulation of prolactin and an inhibitory role in the regulation of GH secretion.
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ABSTRACT
Rat hypothalamic GH-releasing factor (rhGRF), at doses between 0·1 and 10 μg/kg, increased plasma GH concentrations in immature domestic fowl 5–10 min after i.v. injection. Sodium pentobarbitone anaesthesia blunted the GH responses to rhGRF, although in both conscious and anaesthetized chicks the maximal responses were induced by a dose of 1 μg rhGRF/kg. The stimulatory effect of rhGRF on in-vivo GH secretion was less than that provoked by corresponding doses of human pancreatic GRF, but greater than that elicited by two rhGRF analogues, (Nle27)-rhGRF(1–32) and (Nle27)-rhGRF(1–29). These results demonstrate that the chicken pituitary is responsive to mammalian GRF and provide evidence of structure-activity relationships of GRF in the domestic fowl.
J. Endocr. (1986) 108, 413–416
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The concentrations of both GH and prolactin in the circulation of the domestic fowl have been determined after various treatments known to affect carbohydrate metabolism. Fasting decreased the level of glucose, stimulated the secretion of GH and inhibited the secretion of prolactin. Administration of insulin significantly depressed the level of GH in the plasma of normal or fasted birds and also in chickens which had received simultaneous injections of glucose or 2-deoxy-d-glucose. No consistent effect of insulin on the secretion of prolactin was observed. Hyperglycaemia subsequent to administration of glucose had no effect on the levels of either GH or prolactin. Glucagon-induced hyperglycaemia suppressed the level of GH in the plasma and stimulated that of prolactin.