The relation between maternal restraint and food deprivation, plasma corticosterone, and induction of cleft palate in the offspring of mice

Teratology ◽  
1975 ◽  
Vol 12 (2) ◽  
pp. 97-103 ◽  
Author(s):  
Susan M. Barlow ◽  
Patricia R. McElhatton ◽  
Frank M. Sullivan
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


2017 ◽  
Vol 51 (1) ◽  
pp. 134-141 ◽  
Author(s):  
Alison C. Webb ◽  
Lacy D. Chick ◽  
Vincent A. Cobb ◽  
Matthew Klukowski

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.


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.


1981 ◽  
Vol 1 (1) ◽  
pp. 53-63 ◽  
Author(s):  
M.M.A. Elmazar ◽  
Patricia R. McElhatton ◽  
F.M. Sullivan

1 In Charles River CD 1 mice, a single dose of 100 mg kg-1 caffeine injected intraperitoneally on day 14 of pregnancy caused a low incidence of cleft palate in the fetuses. 2 Single oral doses of caffeine of 200 and 300 mg kg-1 but not 100 mg kg-1 on day 14, caused cleft palate in some of the fetuses, but was clearly toxic to the dams. 3 Oral doses of caffeine up to 300 mg kg-1 on day 14 of pregnancy did not reduce utero-placental blood flow, placental transfer function, or amniotic fluid volume. 4 An oral dose of 100 mg kg-1 caffeine induced a marked stimulation of adrenocortical secretion producing plasma corticosterone levels of 1248 ± 129 ?g per 100 ml by 2 h and with elevated levels persisting more than 8 h. 5 It is suggested that the elevated plasma corticosterone is the cause of the cleft palate induced in mice by caffeine. Since corticosterone is a known cleft palate inducer in mice but not in man these results do not predict a hazard from normal caffeine consumption in man.


1994 ◽  
Vol 266 (4) ◽  
pp. E606-E611
Author(s):  
M. Mitome ◽  
S. Honma ◽  
T. Yoshihara ◽  
K. Honma

Extracellular norepinephrine (NE) in the vicinity of the paraventricular nucleus was continuously measured over 24 h by means of in vivo microdialysis in rats under restricted daily feeding and ad libitum feeding. A 24-h rhythm in plasma corticosterone was monitored in separate rats under identical conditions. Under ad libitum feeding, the paraventricular NE showed a 24-h rhythm with lower levels in the light period and higher levels in the dark period. The temporal pattern was not affected by food deprivation for 3 days. The circadian peak of paraventricular NE lagged slightly behind that of plasma corticosterone under ad libitum feeding. On the other hand, when rats were fed for 2 h at a fixed time of day for 3 wk, the NE rhythm was changed and showed a major peak just before daily meals. To examine the nature of the prefeeding NE peak, a 24-hour variation of paraventricular NE was measured in rats under food deprivation that had been subjected to restricted daily feeding for 3 wk and subsequently to ad libitum feeding for 7 days. The paraventricular NE was high around the time when meal had been supplied under restricted daily feeding and low in the dark period. Similar changes were observed in plasma corticosterone. The findings indicate that the prefeeding increase in the paraventricular NE release is regulated by a feeding-associated circadian rhythm manifest in rats under restricted daily feeding.


1975 ◽  
Vol 6 (3) ◽  
pp. 119-124 ◽  
Author(s):  
Robert T. Wertz ◽  
Michael D. Mead

Typical examples of four different speech disorders—voice, cleft palate, articulation, and stuttering—were ranked for severity by kindergarten, first-grade, second-grade, and third-grade teachers and by public school speech clinicians. Results indicated that classroom teachers, as a group, moderately agreed with speech clinicians regarding the severity of different speech disorders, and classroom teachers displayed significantly more agreement among themselves than did the speech clinicians.


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