Drinking-induced changes in fowl adrenocortical activity: effect of visual and non-visual stimuli

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

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.


2019 ◽  
Vol 19 (1S) ◽  
pp. 159-160
Author(s):  
G M Aleshina

The effect of various structural variants of human lactoferrin on stress-induced changes in the corticosterone level in the blood in rats was studied. A model of combined emotional and physical stress - swimming in cold water (1-4 °C) for 2 minutes. The level of corticosterone in plasma was determined by enzyme immunoassay. We have previously found that preventive intraperitoneal administration of native lactoferrin reduces the stress-induced increase in corticosterone concentration in the blood of rats 30 minutes after stress. This work shows that transgenic human lactoferrin, which lacks four arginine residues at the N-terminus, does not have this effect. The obtained results allow us to conclude about the key role of N-terminal amino acid residues in the implementation of the corticostatic activity of lactoferrin.


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.


1978 ◽  
Vol 79 (3) ◽  
pp. 405-406 ◽  
Author(s):  
A. VALETTE ◽  
G. CARASCO ◽  
A. VÉRINE ◽  
L. VARÉSI ◽  
J. BOYER

Service d'Explorations Métaboliques, Hôpital de la Conception, 13385 Marseille Cedex 4, France (Received 24 July 1978) It has recently been shown that ethynyl oestradiol markedly decreases lipase activity in the liver (Valette, Verine, Salers & Boyer, 1977). These observations, along with reports of oestrogen receptors in the liver (Chamness, Costlow & McGuire, 1975) suggest that oestrogens exert considerable influence over the hepatic metabolism of lipids. Previous investigations (DeLorimier, Gordon, Lowe & Carbone, 1965; Gallagher, Mueller & Kappas, 1966) have suggested that the extent of the hepatic changes could be correlated with the molecular nature of the hormonal compound and might depend particularly on the 17α-alkyl-substituted group in synthetic oestrogens. The influence of the ethynyl function in the 17α-position of oestradiol-17β on the oestrogen-induced changes observed in hepatic lipases and serum levels of triglycerides has therefore been examined. Adult female Sprague–Dawley rats (220–240 g) were allowed free access to food and


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.


1980 ◽  
Vol 32 (3) ◽  
pp. 459-472 ◽  
Author(s):  
T. J. Roper

In Experiment I rats deprived of either food or water were given free access to food or water respectively, and their behaviour was observed during self-imposed pauses in feeding or drinking. In Experiment II food or water were delivered according to fixed-time 30-s and fixed-time 60-s schedules, and the behaviour of the rats was observed during the interreinforcement intervals imposed by these schedules. In both experiments the temporal pattern of those activities that occurred during pauses in eating differed from the pattern of activities occurring during pauses in drinking; and with both food and water the temporal pattern of activities during self-imposed pauses in consummatory behaviour in Experiment I proved a good predictor of the pattern of activities during schedule-imposed interreinforcement intervals in Experiment II. This suggests that intermittent schedules permit the occurrence of those activities that are normally closely associated with the consummatory behaviour in question. In Experiment II certain activities that occurred towards the end of the interreinforcement interval were found to be enhanced relative to baseline level, but there was no enhancement of activities occurring near the beginning of the interval. This is contrary to Staddon's (1977) account of schedule-induced behaviour, and suggests that schedule-induction is not as common as has sometimes been supposed.


1959 ◽  
Vol 196 (5) ◽  
pp. 965-968 ◽  
Author(s):  
Clarence Cohn ◽  
Dorothy Joseph

Normal young adult male rats were either force-fed or allowed to eat ad libitum a moderate carbohydrate diet for 3–4 weeks. The force-fed animals were given either the amount of diet consumed by the animals eating ad libitum (pair-fed) or 80% of this amount (underfed). After a 2-week period of observation, we found that the rats eating ad libitum gained 65 gm of body weight, the pair-fed, force-fed 62 gm and the underfed, force-fed 40 gm. On the basis of the water, fat and protein content of the skin, viscera and carcass of control animals killed at the beginning of the feeding regimen and of similar constituents of the experimental animals after 2 weeks of feeding, the composition of the newly formed tissues of the various groups of animals consisted of the following: a) the rat with free access to food—water = 67.8%, fat = 7.8% and protein = 22.4%; b) the pair-fed, force-fed animal—water = 55.5%, fat = 23.6% and protein = 17.7%; c) the underfed, force-fed animal—water = 64.4%, fat = 7.9% and protein = 20.0%. The ratio of calories retained in newly formed tissue to the calories ingested over the 2-week period was 11.9% for the animals eating ad libitum, 20.6% for the pair-fed, force-fed animals and 9.5% for the underfed, force-fed rats. Force feeding appears to change intermediary metabolic pathways in the direction of increased ‘efficiency’ with resultant greater fat deposition.


Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1367 ◽  
Author(s):  
Claudia Romano ◽  
Giovanni Corsetti ◽  
Vincenzo Flati ◽  
Evasio Pasini ◽  
Anna Picca ◽  
...  

An adequate intake of essential (EAA) and non-essential amino acids (NEAA) is crucial to preserve cell integrity and whole-body metabolism. EAA introduced with diet may be insufficient to meet the organismal needs, especially under increased physiological requirements or in pathological conditions, and may condition lifespan. We therefore examined the effects of iso-caloric and providing the same nitrogenous content diets, any diet containing different stoichiometric blends of EAA/NEAA, on mouse lifespan. Three groups of just-weaned male Balb/C mice were fed exclusively with special diets with varying EAA/NEAA ratios, ranging from 100%/0% to 0%/100%. Three additional groups of mice were fed with different diets, two based on casein as alimentary proteins, one providing the said protein, one reproducing the amino acidic composition of casein, and the third one, the control group, was fed by a standard laboratory diet. Mouse lifespan was inversely correlated with the percentage of NEAA introduced with each diet. Either limiting EAA, or exceeding NEAA, induced rapid and permanent structural modifications on muscle and adipose tissue, independently of caloric intake. These changes significantly affected food and water intake, body weight, and lifespan. Dietary intake of varying EAA/NEAA ratios induced changes in several organs and profoundly influenced murine lifespan. The balanced content of EAA provided by dietary proteins should be considered as the preferable means for “optimal” nutrition and the elevated or unbalanced intake of NEAA provided by food proteins may negatively affect the health and lifespan of mice.


1990 ◽  
Vol 258 (1) ◽  
pp. E65-E70 ◽  
Author(s):  
A. R. Gwosdow ◽  
M. S. Kumar ◽  
H. H. Bode

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)


1994 ◽  
Vol 267 (4) ◽  
pp. R901-R908 ◽  
Author(s):  
R. D. Reidelberger ◽  
G. Varga ◽  
R. M. Liehr ◽  
D. A. Castellanos ◽  
G. L. Rosenquist ◽  
...  

A cholecystokinin monoclonal antibody (CCK MAb) was used to immunoneutralize CCK to test the hypothesis that CCK produces satiety by an endocrine mechanism. We first characterized the effects of CCK MAb on pancreatic secretion. Conscious rats with jugular vein and bile-pancreatic duct cannulas received CCK MAb or control antibody intravenously 30 min before a 2-h maximal dose of CCK-8 (200 pmol.kg-1.h-1 i.v.) or access to food. CCK MAb caused dose-related inhibition of amylase secretion. CCK MAb (2 mg/kg) completely blocked the response to CCK-8 and inhibited the response to food by 89%. In feeding experiments, rats with free access to food received CCK MAb or control antibodies (2 mg/kg iv) 2 h after lights off. CCK MAb had no effect on 1.5- or 3.5-h food intake. Another group of rats received CCK MAb (4 mg/kg i.v.) or a combined injection of type A and type B CCK receptor antagonists devazepide and L-365,260 (1 mg/kg each i.v.). CCK MAb had no effect on feeding, whereas the receptor antagonists stimulated 1-, 2-, 3-, and 4-h intake by 62, 45, 43, and 29%. These results suggest that endogenous CCK stimulates pancreatic enzyme secretion at least partially by an endocrine mechanism and produces satiety by a nonendocrine mechanism.


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