Reduced adrenocortical function and increased thyroid function in fasted and refed chickens

1983 ◽  
Vol 98 (1) ◽  
pp. 129-135 ◽  
Author(s):  
S. Harvey ◽  
H. Klandorf

The deprivation of food for 48 h markedly increased (P< 0·001) the corticosterone concentration in the plasma of 7- to 8-week-old chickens. When fasted birds were refed for 2 min or 5 s the corticosterone concentration fell to the level in fed birds within 30 min of refeeding. In fasted and refed birds the plasma corticosterone concentration remained lowered for at least 150 min after a 2-min period of refeeding, whereas in birds refed for 5 s the concentration had increased within 120 min to that in fasted birds. When fasted birds were refed 1, 5, 15 or 30 g diet the corticosterone level was again markedly reduced (P< 0·001) within 45 min of refeeding. The magnitude of this post-feeding decline was unrelated to the amount of food eaten, although its duration was; the level in birds refed 1, 5 or 15 g food increasing to that in fasted birds within 90, 135 and 225 min respectively. The corticosterone level in birds refed 30 g diet remained reduced for at least 225 min but increased to that in fasted birds 24 h after refeeding. The initial decline in the corticosterone concentration was unrelated to the consumption of food, since a similar reduction in the corticosterone level was observed in fasted birds which were given the sight of food but prevented from eating it by Perspex lids attached to the food troughs. This initial decline in the corticosterone level was not a result of stress, as it did not occur in fasted control birds. These results suggest that the adrenocortical changes in fasted and refed birds is initially mediated by a conditioned neural stimulus (reinforcement) and is maintained as a result of peripheral metabolic effects of ingested food. In fasted chickens the concentration of plasma tri-iodothyronine (T3) was greatly reduced (P<0·001) in comparison with fed birds. When fasted birds were refed for 2 min or with 5, 15 or 30 g diet, the level of plasma T3 was increased (P < 0·05) 90 min after refeeding although not to the level in birds which had free access to food. The magnitude and duration of this increase was related to the amount of food consumed and was not observed in birds refed for 5 s or with 1 g food or in fasted birds given sight of but not access to food.

1985 ◽  
Vol 104 (2) ◽  
pp. 225-231 ◽  
Author(s):  
S. Harvey ◽  
H. Klandorf ◽  
S.-K. Lam

ABSTRACT The deprivation of drinking water for 30 h resulted in increased corticosterone concentrations in the plasma of 8- to 10-week-old chickens. When water-deprived birds were allowed to drink ad libitum the corticosterone concentration declined within 45 min, to the level in hydrated controls, and remained suppressed thereafter. Similar reductions in the corticosterone concentrations were also observed in water-deprived chicks which were allowed to drink for only 5 min, 1 min or 5 s. The involvement of visual stimuli in mediating this adrenocortical response was demonstrated by a comparable decline in the corticosterone concentration in water-deprived birds which were presented with water but not allowed access to it. Non-visual stimuli also appeared to be causally involved in the adrenocortical suppression after drinking, since the intraperitoneal injection of tap water (40 ml per bird) also resulted in a lowering of the corticosterone level. However, in the absence of appropriate reinforcement from metabolic stimuli, a rebound in the corticosterone concentration was observed in birds prevented from drinking, in birds unable to satiate their thirst and in birds rehydrated (orally or intraperitoneally) without feeding. These results demonstrate adrenocortical suppression in water-deprived chickens after free access to food and water and the involvement of visual and non-visual stimuli in mediating this response. The maintenance of adrenocortical suppression is dependent upon metabolic stimuli associated with food and water intake. J. Endocr. (1985) 104, 225–231


1988 ◽  
Vol 116 (2) ◽  
pp. 179-183 ◽  
Author(s):  
A. Cheung ◽  
S. Harvey ◽  
T. R. Hall ◽  
S.-K. Lam ◽  
G. S. G. Spencer

ABSTRACT Young cockerels (6–8 weeks old) were injected with serum from sheep immunized against somatostatin-14 (anti-SRIF) or normal sheep serum (NSS). Blood samples were withdrawn periodically for the determination of plasma corticosterone concentration by radioimmunoassay. With frequent (every 10 min) sampling, NSS-treated control animals exhibited increased plasma corticosterone levels, presumably as a stress response to the experimental manipulation. Anti-SRIF stimulated a much greater increase in plasma corticosterone concentrations and a peak response was observed within 10 to 20 min, when the plasma corticosterone level reached more than twice that of the corresponding control value. With less frequent sampling, plasma corticosterone increased with anti-SRIF administration to as much as nine times the corresponding control value, and the peak response occurred much later. Under pentobarbitone anaesthesia, which itself increased basal corticosterone concentrations, anti-SRIF treatment promoted further increases in plasma corticosterone levels although to a smaller magnitude compared with conscious birds. The results suggest that endogenous somatostatin may play a role in the regulation of adrenocortical function in the domestic fowl. The mechanism of response may involve a central component. J. Endocr. (1988) 116, 179–183


1992 ◽  
Vol 262 (6) ◽  
pp. E948-E955 ◽  
Author(s):  
K. Honma ◽  
Y. Noe ◽  
S. Honma ◽  
Y. Katsuno ◽  
T. Hiroshige

Effects of local destruction of the brain catecholaminergic neurons were examined on the light- and feeding-associated circadian rhythms in plasma corticosterone in rats. 6-Hydroxydopamine (6-OHDA), a selective and long-lasting neurotoxin of the catecholaminergic neurons, was microinjected into the following discrete areas of the brain: the paraventricular nucleus (PVN), median eminence (ME), suprachiasmatic nucleus (SCN), ventromedial hypothalamic nucleus (VMH), lateral hypothalamic nucleus (LH), and the ascending bundle of noradrenergic neurons (NAB). And the feeding-associated as well as the light-associated circadian rhythms in plasma corticosterone were determined. The light-associated circadian rhythm was assayed under a 24-h light-dark cycle with free access to food, whereas the feeding-associated circadian rhythm was measured under restricted daily feeding in which rats had free access to food at a fixed time of day. 6-OHDA reduced the norepinephrine concentrations in respective regions to 10-30% of the control value, except for the LH. The light-associated circadian rhythm was not affected by 6-OHDA into the SCN or PVN. By contrast, 6-OHDA into the PVN or ventral NAB suppressed the feeding-associated circadian peak. 6-OHDA into the VMH and LH showed some effects on plasma corticosterone level but not on the feeding-associated circadian rhythm. 6-OHDA had no systematic effect on plasma corticosterone level when injected into the SCN, ME, and dorsal NAB. These findings indicate that the catecholaminergic neurons projecting to the PVN are involved in the feeding-associated but not in the light-associated circadian rhythms.


1981 ◽  
Vol 241 (1) ◽  
pp. R21-R24 ◽  
Author(s):  
R. G. Doell ◽  
M. F. Dallman ◽  
R. B. Clayton ◽  
G. D. Gray ◽  
S. Levine

These experiments were undertaken to investigate the mechanism whereby a precipitous drop in plasma corticosterone concentration is brought about following drinking in rats on a restricted water schedule. No alteration in adrenocorticotrophic hormone (ACTH) output was found, nor was catabolism of corticosterone sufficient to account for the drop. It is concluded that corticosterone level is controlled under these conditions by a mechanism independent of ACTH concentration.


1977 ◽  
Vol 43 (5) ◽  
pp. 839-843 ◽  
Author(s):  
J. A. Severson ◽  
R. D. Fell ◽  
J. G. Tuig ◽  
D. R. Griffith

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone were determined in exercise-trained rats. Rats, 100, 200, and 300 days of age, were trained for a 10-wk period by treadmill running. Following the training program, rats were subjected to an acute bout of swimming. Acute swimming elevated plasma corticosterone concentrations in all age groups. At 170 days of age, the plasma corticosterone concentration following swimming was higher in exercise-trained rats than in controls. The opposite was true of acutely swum rats at 270 and 370 days of age. Acute swimming elevated the in vitro adrenal gland response to adrenocorticotropic hormone stimulation in control rats at all ages and in trained rats at 170 days of age. The in vivo relationship of epinephrine and the pituitary adrenal system is suggested as a mechanism which could have caused this response. The relationship of secretion rates to plasma corticosterone concentrations indicated that extra-adrenal mechanisms, such as decreased turnover, were also responsible for the elevated plasma corticosterone levels observed in response to acute swimming.


1988 ◽  
Vol 119 (3) ◽  
pp. 339-344 ◽  
Author(s):  
Jon D. Dunn ◽  
Jerald J. Killion

Abstract. We previously have shown that melittin evokes a sustained increase in plasma corticosterone levels of the female rat. Significant increases occurred only during the morning and the duration of the response was increased from 48 h to 8 days by a second milittin injection 3 days after initial exposure to melittin. To further evaluate the effect of melittin on adrenocortical function, rats were given melittin at 09.00 h on days 1 and 4 and on day 8 rats were subjected to a variety of different stresses. Saline-injected rats served as controls. Blood for determining non-stress and stress levels of corticosterone concentration (RIA) was collected by decapitation. In all cases morning but not afternoon non-stress plasma corticosterone levels of melittin-injected rats were higher than those of saline-injected controls; afternoon non-stress corticosterone levels did not differ between groups. Melittin- and saline-treated rats showed comparable corticosterone responses to a morning 2-min restraint stress. In contrast, melittin treatment facilitated the pituitary-adrenal response to rotational and surgical stress as well as the stress of removing one rat from a cage of two. Fifteen min after removal of the first rat of a cage of two, plasma corticosterone levels of the melittin-injected rat were significantly higher than those of saline-injected rats. Likewise, plasma corticosterone levels of melittin-treated rats were higher (P < 0.05) than those of saline-injected rats 15 min after rotational (10 rpm) and surgical (jugular cutdown and blood withdrawal) stress. Collectively these data indicate that exposure to melittin (and/or the resulting increase in morning corticosterone levels) may have a significant influence on the pituitary-adrenal responsiveness to stress.


1992 ◽  
Vol 127 (5) ◽  
pp. 471-475 ◽  
Author(s):  
Edmund Przegaliński ◽  
Bogusława Budziszewska ◽  
Anna Grochmal

In this study we examined the effect of the adenosine analogues: N6-cyclohexyladenosine, L-N6-phenylisopropyladenosine and 5′-N-ethylcarboxamidoadenosine on the plasma corticosterone concentration in rats. It was found that N6-cyclohexyladenosine (0.1–3.0 mg/kg), L-N6-phenylisopropyladenosine (0.1–1.0 mg/kg) and 5′-N-ethylcarboxamidoadenosine (0.01–1.0 mg/kg) dose-dependently increased the plasma corticosterone level. The effects of N6-cyclohexyladenosine (0.1 mg/kg) and L-N6-phenylisopropyladenosine (0.1 mg/kg) were completely blocked in animals pretreated with dexamethasone (3 × 1 mg/kg), as well as in animals with a pharmacological blockade of the release of hypothalamic corticotropin-releasing factor induced by chloropromazine (10 mg/kg), morphine (20 mg/kg) and nembutal (25 mg/kg), whereas the corticosterone response to 5′-N-ethylcarboxamidoadenosine (0.01 mg/kg) was blocked in dexamethasone-pretreated rats only. On the other hand, the adenosine receptor antagonists: 8-(p-sulfophenyl)-theophylline (30 mg/kg), 8-phenyltheophylline (10 and 30mg/kg), 1,3-dipropyl-8-(2-amino-4-chloro)-phenylxanthine (1 and 3 mg/kg) and 1,3-dipropyl-7-methylxanthine (1 mg/kg) did not affect the corticosterone response to N6-cyclohexyladenosine, L-N6-phenylisopropyladenosine or 5′-N-ethylcarboxamidoadenosine. The obtained results indicate that N6-cyclohexyladenosine and L-N6-phenylisopropyladenosine stimulate the corticosterone secretion at the hypothalamic level, whereas 5′-N-ethylcarboxamidoadenosine is likely to act at the pituitary level. Although the effects produced by the adenosine analogues show that both A1 and A2 receptors are involved in the corticosterone response, negative results of the interaction studies with adenosine receptor antagonists indicate that further experiments are necessary to elucidate this problem.


1971 ◽  
Vol 49 (3) ◽  
pp. 437-457 ◽  
Author(s):  
E. L. BRADLEY ◽  
W. N. HOLMES

SUMMARY The general effect of chronic hypophysectomy on organ and body weights, liver glycogen, blood glucose, peripheral plasma corticosterone concentrations, and blood pressure in the duck were similar to those described for several mammalian species. The disappearance and distribution of radioactivity after the administration of [1,2-3H]corticosterone and [1,2-3H]aldosterone was studied according to a single compartment model system. When compared with sham-operated ducks, the apparent volumes of distribution and the biological half-lives of radioactivity in hypophysectomized ducks were significantly increased, and the estimated metabolic clearance rates of [1,2-3H] corticosterone and [1,2-3H]aldosterone were significantly decreased. The patterns of distribution of radioactivity and the rate of metabolism of both hormones returned towards normal when the chronically hypophysectomized ducks were treated with corticotrophin (ACTH). Fourteen days after hypophysectomy the peripheral plasma concentration of corticosterone and the estimated rate of corticosterone secretion by the adrenal fell to 10 and 4%, respectively, of the values observed in sham-operated birds. Examinations of the peripheral plasma corticosterone concentration during the first 30 min after the removal of the adenohypophysis indicated a mean biological half-life for endogenous corticosterone of 13·7 min. The rates of appearance of radioactivity in the bile, intestine and cloaca of the hypophysectomized birds suggested substantial declines in the rates of aldosterone and corticosterone metabolism. These declines could not be accounted for by the reduced rate of glomerular filtration in the hypophysectomized bird. Replacement therapy with ACTH restored the excretory patterns of both steroids towards normal. The quantitative similarities between the effects of hypophysectomy in the duck and several mammalian species make it unnecessary to postulate either a high degree of adrenal autonomy or an extrahypophysial source of ACTH in the control of adrenocortical function in the duck.


1968 ◽  
Vol 46 (4) ◽  
pp. 567-571 ◽  
Author(s):  
E. Stark ◽  
Zs. Ács ◽  
G. B. Makara ◽  
K. Mihály

Twenty-four hours after the last of 14 daily injections of ACTH, the administration of ether, histamine, 1% formalin, or lysine-8-vasopressin produced no rise in the plasma corticosterone level in rats but raised it significantly in saline-treated control animals. As assayed by the plasma corticosterone concentration, ACTH release was found to be inhibited when hypophyseal–adrenocortical responsiveness was not impaired and the peripheral corticosterone level was normal or less than normal. Endotoxin induced nearly the same statistically significant elevation in the ACTH-treated and saline-treated animals. It would appear that it is the high corticosterone level produced by the last ACTH injection that suppresses the corticotrophin-releasing factor (CRF) 24 h later (feedback action) when this level returns to normal or less than normal; and that certain stressors liberate CRF whereas others do not. An explanation for the latter assumption may be found either in the difference in intensity between the stimuli or, more probably, in that the high corticosterone level inhibits the ACTH release mechanism for certain individual stressors, but not for others.


2001 ◽  
Vol 47 (1) ◽  
pp. 34-36
Author(s):  
V. V. Bulygina ◽  
L. N. Maslova ◽  
A. L. Markel

Functional activity of the hypothalamo-pituitary-adrenocortical system (HPAS) was evaluated over time in rats with hereditary stress-induced arterial hypertension (HSIAH) and normotensive Wistar rats. Peripheral blood plasma corticosterone was measured in rats aged 2, 3, 4, 6, 8, 10, 12, and 18 weeks at rest and after 1-h immobilization in perforated cylinders by competitive protein binding. Basal corticosterone level and HPAS reaction to stress were lower in hypertensive rats than in Wistar rats of the same age. The only exclusion was the age of 4 weeks, when hypertension starts to form in HSIAH rats and their HPAS is more sensitive to emotional stress than that of Wistar rate, this sensitivity being associated with increased adrenal reaction to ACTH. Decreased HPAS reaction to emotional stress in adult HSIAH rats was not associated with disorders in adrenal sensitivity to ACTH.


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