Effects of Moderate Food Deprivation on Plasma Corticosterone and Blood Metabolites in Common Watersnakes (Nerodia sipedon)

2017 ◽  
Vol 51 (1) ◽  
pp. 134-141 ◽  
Author(s):  
Alison C. Webb ◽  
Lacy D. Chick ◽  
Vincent A. Cobb ◽  
Matthew Klukowski
1990 ◽  
Vol 36 (3) ◽  
pp. 451-456 ◽  
Author(s):  
Joseph R. Coveney ◽  
Bethany S. Neal ◽  
Sheldon B. Sparber

1995 ◽  
Vol 145 (1) ◽  
pp. 143-153 ◽  
Author(s):  
G A C van Haasteren ◽  
E Linkels ◽  
W Klootwijk ◽  
H van Toor ◽  
J M M Rondeel ◽  
...  

Abstract The purpose of this study was to investigate the mechanisms involved in the reduced thyroid function in starved, young female rats. Food deprivation for 3 days reduced the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA, the amount of proTRH-derived peptides (TRH and proTRH160–169) in the paraventricular nucleus, the release of proTRH-derived peptides into hypophysial portal blood and the pituitary levels of TSHβ mRNA. Plasma TSH was either not affected or slightly reduced by starvation, but food deprivation induced marked increases in plasma corticosterone and decreases in plasma thyroid hormones. Refeeding after starvation normalized these parameters. Since the molar ratio of TRH and proTRH160–169 in hypophysial portal blood was not affected by food deprivation, it seems unlikely that proTRH processing is altered by starvation. The median eminence content of pGlu-His-Pro-Gly (TRH-Gly, a presumed immediate precursor of TRH), proTRH160–169 or TRH were not affected by food deprivation. Since median eminence TRH-Gly levels were very low compared with other proTRH-derived peptides it is unlikely that α-amidation is a rate-limiting step in hypothalamic TRH synthesis. Possible negative effects of the increased corticosterone levels during starvation on proTRH and TSH synthesis were studied in adrenalectomized rats which were treated with corticosterone in their drinking water (0·2 mg/ml). In this way, the starvation-induced increase in plasma corticosterone could be prevented. Although plasma levels of thyroid hormones remained reduced, food deprivation no longer had negative effects on hypothalamic proTRH mRNA, pituitary TSHβ mRNA and plasma TSH in starved adrenalectomized rats. Thus, high levels of corticosteroids seem to exert negative effects on the synthesis and release of proTRH and TSH. This conclusion is corroborated by the observation that TRH release into hypophysial portal blood became reduced after administration of the synthetic glucocorticosteroid dexamethasone. On the basis of these results, it is suggested that the reduced thyroid function during starvation is due to a reduced synthesis and release of TRH and TSH. Furthermore, the reduced TRH and TSH synthesis during food deprivation are probably caused by the starvation-induced enhanced adrenal secretion of corticosterone. Journal of Endocrinology (1995) 145, 143–153


1983 ◽  
Vol 245 (3) ◽  
pp. R339-R344 ◽  
Author(s):  
K. I. Honma ◽  
S. Honma ◽  
T. Hiroshige

The effects of food on plasma corticosterone levels were examined in rats under restricted daily feeding or prolonged food deprivation. High hormone levels before feeding were observed when the daily meal was restricted to 2 h at a fixed time of day, but it was not detected when food availability was extended to 6 h. The amount of food intake under the latter condition was comparable to that in 24 h of ad libitum feeding. After the termination of restricted feeding, the prefeeding hormone peak was maintained in rats fasted subsequently but disappeared when rats were returned to ad libitum feeding. Food deprivation for 10 days increased plasma corticosterone levels in the light period, resulting in abolition of the circadian rhythm. A subsequent meal decreased the hormone level such that the 24-h mean hormone level after food ingestion was inversely related to the amount of food intake. When rats were allowed to feed for 6 h after prolonged food deprivation, the prefeeding hormone peak observed at the second meal disappeared at the fourth meal. The amount of food consumption in these rats increased and reached a level comparable to that with ad libitum feeding at the third meal. It is concluded that the amount of food intake is critical for the development and maintenance of the prefeeding hormone peak under restricted feeding; prolonged fasting.


1975 ◽  
Vol 66 (1) ◽  
pp. 93-99 ◽  
Author(s):  
SUSAN M. BARLOW ◽  
P. J. MORRISON ◽  
F. M. SULLIVAN

SUMMARY Plasma corticosterone levels were measured in the pregnant and non-pregnant mouse after acute and chronic stress. Acute surgical stress in the non-pregnant mouse increased plasma corticosterone from a mean resting level of 2·3 to 50·6 μg/100 ml 1 h after operation. By 24 h after operation, levels had fallen back to 7·6 μg/100 ml. In the pregnant mouse an acute surgical stress on day 14 of pregnancy increased plasma corticosterone levels to 525 μg/100 ml 1 h after surgery from a resting value of 80 μg/100 ml, with a return to resting levels by 24 h. During the chronic stress of 24 h restraint, plasma corticosterone levels in the non-pregnant mouse reached a peak (81·0 μg/100 ml) 1 h after the start of restraint and were still raised (mean 24·0 μg/100 ml) after 24 h. In the pregnant restrained mouse a peak value of 733 μg/100 ml was seen at 1 h, with levels maintained at around 500–600 μg/100 ml during the next 16 h of restraint. Increased levels of 268 μg/100 ml were still present at 24 h. After the chronic stress of 24 h food deprivation, plasma corticosterone levels in the non-pregnant and pregnant mice were raised after 7 h to levels slightly lower than those observed in the restrained groups, and at 24 h levels in the respective restrained and fooddeprived groups were similar, suggesting that food deprivation is a powerful chronic stressor in the mouse. During chronic stress in the pregnant mouse where plasma corticosterone levels of around 600 μg/100 ml were maintained for some hours, protein binding studies indicated that 10 μg/100 ml was free, unbound corticosterone. The physiological and pathological consequences of such high levels of free corticosterone during stress in pregnancy are discussed.


1986 ◽  
Vol 238 (3) ◽  
pp. 811-816 ◽  
Author(s):  
D G Clark ◽  
S D Neville ◽  
M Brinkman ◽  
P V Nelson ◽  
R J Illman ◽  
...  

The effects of food deprivation on body weight, liver weight, hepatic glycogen content, glycogenolytic enzymes and blood metabolites were compared in young and old phosphorylase b kinase-deficient (gsd/gsd) rats. Although the concentration of glycogen in liver from 9-week-old female gsd/gsd rats (730 mumol of glucose equivalents/g wet wt.) was increased by 7-8% during starvation, total hepatic glycogen was decreased by 12% after 24 h without food. In 12-month-old male gsd/gsd rats the concentration of liver glycogen (585 mumol of glucose equiv./g wet wt.) was decreased by 16% and total hepatic glycogen by nearly 40% after food deprivation for 24 h. Phosphorylase b kinase and phosphorylase a were present at approx. 10% of the control activities in 9-week-old gsd/gsd rats, but both enzyme activities were increased more than 3-fold in 12-month-old affected rodents. It is concluded that the age-related ability to mobilize hepatic glycogen appears to result from the augmentation of phosphorylase b kinase during maturation of the gsd/gsd rat.


1996 ◽  
Vol 271 (2) ◽  
pp. E239-E245 ◽  
Author(s):  
T. Yoshihara ◽  
S. Honma ◽  
Y. Katsuno ◽  
K. Honma

Extracellular neuropeptide Y (NPY) in the vicinity of the paraventricular nucleus (PVN) as well as NPY concentrations in the PVN were measured in rats under ad libitum feeding and 2-day and 10-day food deprivation. Plasma corticosterone levels were not changed by 2-day food deprivation but were increased by subsequent refeeding. In contrast, the extracellular NPY levels were increased by 2-day food deprivation and were decreased rapidly by refeeding. The NPY concentrations were also increased and increased further by refeeding. On the other hand, plasma corticosterone levels were elevated by 10-day food deprivation and were decreased by subsequent refeeding. The extracellular NPY levels were also increased by food deprivation and decreased gradually after refeeding. However, the postprandial levels were still elevated when plasma corticosterone levels were returned to the basal levels. The NPY concentrations were also increased and increased further by refeeding. The amount of food intake after refeeding was positively correlated with the extracellular NPY levels. It is concluded that extracellular NPY levels in the PVN do not necessarily covariate with plasma corticosterone levels in rats under food deprivation.


1996 ◽  
Vol 270 (6) ◽  
pp. R1250-R1256 ◽  
Author(s):  
C. R. Park ◽  
L. Benthem ◽  
R. J. Seeley ◽  
M. I. Friedman ◽  
C. W. Wilkinson ◽  
...  

Using respiratory quotient as an index of metabolic state, we compared the effects of administrations of the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) at a dose of 300 mg/kg with the effect of 10 h of food deprivation. We measured behavioral and physiological responses of the animals receiving the two treatments, including food intake, energy expenditure, rates of carbohydrate and fatty acid utilization, and plasma levels of glucose, insulin, corticosterone, epinephrine, and norepinephrine. A vehicle-treated control group was also included. Fasting produced a greater food intake than 2,5-AM administration. Although plasma glucose, insulin, and norepinephrine levels were similar between the two treatments, plasma corticosterone and epinephrine levels were significantly elevated in animals receiving 2,5-AM. We conclude that although 2,5-AM can produce a metabolic state similar to fasting, as measured by an index of whole body metabolic state (respiratory quotient), there remain factors that influence food intake that are not similar in the two conditions.


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