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The influence of treadmill exercise on corticosterone secretion has been determined in domestic ducks. In birds unused to such exercise the concentrations of plasma corticosterone were markedly increased (> fourfold) after 15 or 30 min of treadmill exercise (1·1 km/h at 3 ° grade) and the level remained high (between 30 and 40 ng/ml) throughout 90 min of exercise. This increase in corticosterone secretion accompanied a similar increase in colon temperature and was independent of the plasma glucose level. After exercise the corticosterone concentration declined to the pretreatment level within 60 min of recovery. In birds used to the exercise the corticosterone response to a standard (30 min) period of exercise was diminished (by 77·6% in comparison with untrained birds and was no greater than the response (1·7-fold) in stationary control birds after handling and bleeding. The diminution of the corticosterone response to exercise may be due to the trained birds becoming fitter and better able to perform the work involved.
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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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Abstract
During the luteal phase in the cow, a first-wave dominant follicle grows to reach ovulatory size, but then ceases to grow, becomes no longer dominant and enters a phase of slow regression. During this growth transition, the concentration of oestradiol has been shown to decrease in follicular fluid. The objective of this study was to determine if follicular fluid oestradiol concentrations are regulated by the activity of three major steroidogenic enzymes, namely P450-aromatase (P450-arom), 3β-hydroxysteroid dehydrogenase/Δ5–Δ4 isomerase (3β-HSD) and 17α-hydroxylase C-17,20 lyase cytochrome P450 enzyme (P450–17α) measured in granulosa and theca cells isolated from individual first-wave dominant follicles. Follicle growth and state of dominance was assessed by ultrasonography and follicles were classified as growing-dominant (GD, n=6), non-growing-dominant (NGD, n=8) or non-growing-non-dominant (NGND, n=6). Mean follicular fluid concentrations of oestradiol were higher in GD than in NGD or NGND follicles (511 ± 98 versus 136 ± 16 and 20 ± 11 nmol/l respectively). Oestradiol was not correlated with P450-arom in any of the three groups. In GD follicles, oestradiol was positively correlated with pregnenolone concentration but neither was correlated with granulosa or theca 3β-HSD activity or with theca P450–17α activity. In NGD follicles, oestradiol was negatively correlated with theca 3β-HSD activity and pregnenolone was negatively correlated with granulosa 3β-HSD activity. In NGND follicles, oestradiol was positively correlated, and pregnenolone was negatively correlated with theca 3β-HSD and P450–17α activities. These studies demonstrated that pregnenolone supply is the principal regulating factor of oestradiol output during follicle dominance and during the loss of dominance but that the levels of P450–17α and 3β-HSD activity become rate-limiting when the follicle is no longer dominant.
Journal of Endocrinology (1996) 149, 233–242
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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.
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Age-related changes in the response of GH to administration of thyrotrophin releasing hormone (TRH) have been investigated in the domestic fowl. In two strains of chicken the i.v. administration of TRH (10 μg/kg) to 4-week-old male and female birds markedly increased (> 200 ng/ml) the plasma GH concentration within 10 min of treatment and the concentration remained higher than the pretreatment level for at least a further 20 min. Saline (0·9%) administration had no effect on GH secretion in comparable groups of control birds. The same dose of TRH had no effect on plasma GH concentrations in adult (> 24-week-old) laying hens or cockerels. The administration of TRH at doses of 0·1–100 μg/kg (i.v.) or 0·39–50 μg/bird (s.c.) also had very little, if any, effect on GH secretion in laying hens. In laying hens slight increases (10–20 ng/ml, P < 0·05) in the plasma concentrations of GH were observed in one experiment 60 min after the s.c. injection of 100 μg TRH, and in another 60, 90 and 120 min after the serial s.c. injection of TRH (100 μg/bird) every 30 min over a 150 min period. The poor GH response of the adults to TRH stimulation was not due to high circulating concentrations of endogenous gonadal steroids, as surgical gonadectomy had no effect on the GH response to TRH. These results suggest maturational differences in the control of GH secretion in the fowl.
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The influence of stress on the secretion of corticosterone has been investigated by radioimmunoassay in domestic ducks (Anas platyrhynchos) of 6–8 weeks of age. Intravenous and i.m. injections of synthetic ACTH (Synacthen, 25 i.u./bird and Synacthen Depot, 100 i.u./bird respectively) markedly increased (2·7- to 10-fold) basal concentrations of corticosterone in plasma (3–6 ng/ml) in comparison with those in birds injected with 0·9% saline (1 ml/bird). Maximum levels of 30–40 ng/ml plasma were reached after 30 min and 5 h respectively. Increased levels of corticosterone in plasma were also seen within 5 min of i.v. administration of saline and remained as high as those in birds treated with Synacthen for at least 20 min after injection. Blood sampling (from the brachial vein) was, by itself, sufficient to increase levels of corticosterone in plasma; a large (twofold) rise being observed as soon as 1 min after initial handling and bleeding, with concentrations of 30–40 ng/ml being found in birds bled 15 times during a period of 14 min. However, in a flock of birds, the alarm created in unhandled birds while others were being bled had no effect on concentrations of corticosterone in plasma. Deprivation of food or water for 24 h also enhanced levels of corticosterone in plasma, as did 24 h of adaptation to 0·2 m-NaCl drinking water. These results have demonstrated the lability of the secretion of corticosterone in response to stress and demonstrated its usefulness as a physiological indicator of stress in ducks.
