Feeding influences plasma cortisol levels during preweaning life in baboons

1990 ◽  
Vol 259 (1) ◽  
pp. R157-R162 ◽  
Author(s):  
D. S. Lewis ◽  
E. M. Jackson
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Cortisol Concentration ◽  
Papio Cynocephalus ◽  
Once Daily ◽  
Plasma Cortisol Concentration ◽  
Feeding Rhythm ◽  
Time Of Feeding ◽  
Trough Levels ◽  
Effect Of Feeding

The effect of feeding on plasma cortisol concentrations was examined in neonate (preweaning), infant (postweaning), and adult baboons (Papio cynocephalus). Neonates were bottle fed four times daily, infants twice daily, and adults once daily. In neonates, plasma cortisol declined within 30 min after feeding. This decline in plasma cortisol was dependent on ingestion of formula and was independent of the time of feeding. During the day, cortisol fluctuations were synchronized with feeding times: peak levels occurred before feeding and trough levels occurred 30-60 min after feeding. Plasma adrenocorticotropic hormone (ACTH) declined within 30 min after feeding but returned to prefeeding levels at 60 min after feeding and did not exhibit significant variation associated with feeding times as did cortisol. The decline in plasma cortisol after feeding in neonates was delayed with increasing age. By 18 wk, the feed-related decline in plasma cortisol was delayed until 60 min after feeding compared with 30 min at age of 8 wk. After weaning, the decline in plasma cortisol after feeding was delayed until 90 min, and there was no effect of feeding in the afternoon on plasma cortisol. Finally, there was no significant decline at all in adult baboons greater than 6 yr of age. These results demonstrate plasma cortisol concentration is associated with feeding in neonates fed formula. The cortisol-feeding rhythm changes before weaning, and after weaning it begins to disappear, until it is completely absent in adults.

scholarly journals Plasma profiles of adrenocorticotropic hormone, cortisol, α-melanocyte-stimulating hormone, and growth hormone in dogs with pituitary-dependent hyperadrenocorticism before and after hypophysectomy

2006 ◽  
Vol 190 (3) ◽  
pp. 601-609 ◽  
Author(s):  
J M Hanson ◽  
H S Kooistra ◽  
J A Mol ◽  
E Teske ◽  
B P Meij
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Pulse Frequency ◽  
Cortisol Concentration ◽  
Melanocyte Stimulating Hormone ◽  
Plasma Cortisol Concentration ◽  
Before And After ◽  
Basal Plasma ◽  
Stimulating Hormone

The 6-h plasma profiles of adrenocorticotropic hormone (ACTH), cortisol, α-melanocyte-stimulating hormone (α-MSH), and GH were studied in 17 dogs with pituitary-dependent hyperadrenocorticism (PDH) before and after hypophysectomy. The aim of the study was to investigate the relation between the hormone profile characteristics and recurrence of PDH after surgery. The hormones were secreted in a pulsatile fashion. The basal plasma cortisol concentration and area under the curve (AUC) for cortisol were significantly higher in the PDH cases than in eight controls. The characteristics of the plasma profiles of ACTH and α-MSH were not significantly different between the PDH cases and the controls. In the PDH cases, less GH was secreted in pulses than in the controls, but the difference was not significant. The basal plasma cortisol concentration, the AUC for ACTH and cortisol, and the pulse frequency of ACTH and cortisol decreased significantly after hypophysectomy for the group of PDH cases. The basal plasma concentrations of ACTH and α-MSH, the AUC for α-MSH, and the characteristics of the plasma GH profiles of the PDH cases remained unchanged after hypophysectomy. No pulses of α-MSH were observed after hypophysectomy. The co-occurrence between the ACTH and cortisol pulses decreased significantly with hypophysectomy. The postoperative pulse frequency of ACTH was the only characteristic with predictive value for the recurrence of PDH after hypophysectomy. The results of this study demonstrate that ACTH, cortisol, α-MSH, and GH are secreted in a pulsatile fashion in dogs with PDH. Hypophysectomy effectively reduces the secretion of ACTH and cortisol. The presence of ACTH pulses after hypophysectomy is a risk factor for the recurrence of hyperadrenocorticism.

Intrauterine growth restriction delays surfactant protein maturation in the sheep fetus

2010 ◽  
Vol 298 (4) ◽  
pp. L575-L583 ◽  
Author(s):  
Sandra Orgeig ◽  
Tamara A. Crittenden ◽  
Ceilidh Marchant ◽  
I. Caroline McMillen ◽  
Janna L. Morrison
Keyword(s):  
Mrna Expression ◽  
Plasma Cortisol ◽  
Surfactant Protein ◽  
Cortisol Concentration ◽  
Plasma Catecholamine ◽  
Fetal Sheep ◽  
C Protein ◽  
Intrauterine Growth ◽  
Plasma Cortisol Concentration ◽  
The Impact

Pulmonary surfactant is synthesized by type II alveolar epithelial cells to regulate the surface tension at the air-liquid interface of the air-breathing lung. Developmental maturation of the surfactant system is controlled by many factors including oxygen, glucose, catecholamines, and cortisol. The intrauterine growth-restricted (IUGR) fetus is hypoxemic and hypoglycemic, with elevated plasma catecholamine and cortisol concentrations. The impact of IUGR on surfactant maturation is unclear. Here we investigate the expression of surfactant protein (SP) A, B, and C in lung tissue of fetal sheep at 133 and 141 days of gestation (term 150 ± 3 days) from control and carunclectomized Merino ewes. Placentally restricted (PR) fetuses had a body weight <2 SD from the mean of control fetuses and a mean gestational PaO2<17 mmHg. PR fetuses had reduced absolute, but not relative, lung weight, decreased plasma glucose concentration, and increased plasma cortisol concentration. Lung SP-A, -B, and -C protein and mRNA expression was reduced in PR compared with control fetuses at both ages. SP-B and -C but not SP-A mRNA expression and SP-A but not SP-B or -C protein expression increased with gestational age. Mean gestational PaO2was positively correlated with SP-A, -B, and -C protein and SP-B and -C mRNA expression in the younger cohort. SP-A and -B gene expression was inversely related to plasma cortisol concentration. Placental restriction, leading to chronic hypoxemia and hypercortisolemia in the carunclectomy model, results in significant inhibition of surfactant maturation. These data suggest that IUGR fetuses are at significant risk of lung complications, especially if born prematurely.

ANTIDIURETIC HORMONE AND CORTICOTROPHIN RELEASE IN MAN

1960 ◽  
Vol 21 (2) ◽  
pp. 171-176 ◽  
Author(s):  
S. SHUSTER
Keyword(s):  
Antidiuretic Hormone ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Release Factor ◽  
Similar Increase ◽  
Rapid Infusion ◽  
Experimental Procedure ◽  
Plasma Cortisol Concentration ◽  
Corticotrophin Release Factor ◽  
Patients With Diabetes

SUMMARY Plasma cortisol concentrations increased after injections of nicotine. This increase was variable and was no greater than that seen after substitution of normal saline for nicotine. Plasma cortisol concentrations did not increase after nicotine in patients with hypopituitarism and after inhibition of corticotrophin release with triamcinolone. It is concluded that the increased plasma cortisol concentration after injection of nicotine was due to non-specific pituitary stimulation associated with the experimental procedure and not due to any direct effect of the nicotine. Nicotine resulted in a similar increase in plasma cortisol in four patients with diabetes insipidus. Neither rapid infusion of hypertonic mannitol nor ingestion of ethanol had a consistent effect on the plasma cortisol concentration. It is therefore concluded that the antidiuretic hormone is not the 'corticotrophin release factor' in man.

Seasonal variation in plasma cortisol concentration during pregnancy and the puerperium

1980 ◽  
Vol 8 (5) ◽  
pp. 587-588 ◽  
Author(s):  
JUDITH M. BAKER ◽  
SHEILA L. HANDLEY ◽  
GILL WALDRON ◽  
T. LESLIE DUNN
Keyword(s):  
Seasonal Variation ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Plasma Cortisol Concentration

The Mean 1300-1600 h Plasma Cortisol Concentration as a Diagnostic Test for Hypercortisolism*

1982 ◽  
Vol 54 (6) ◽  
pp. 1262-1264 ◽  
Author(s):  
URIEL HALBREICH ◽  
BARNETT ZUMOFF ◽  
JACOB KREAM ◽  
DAVID K. FUKUSHIMA
Keyword(s):  
Diagnostic Test ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Plasma Cortisol Concentration ◽  
The Mean

PLASMA CONCENTRATIONS OF CORTISOL IN HYPOPHYSECTOMIZED AND SODIUM CHLORIDE-ADAPTED GOLDFISH (CARASSIUS AURATUS L.)

1974 ◽  
Vol 63 (2) ◽  
pp. 377-387 ◽  
Author(s):  
JACQUELINE PORTHÉ-NIBELLE ◽  
BRAHIM LAHLOU
Keyword(s):  
Sodium Chloride ◽  
Fresh Water ◽  
Plasma Cortisol ◽  
Carassius Auratus ◽  
Plasma Concentrations ◽  
Cortisol Concentration ◽  
Control Fish ◽  
Chloride Solutions ◽  
Sodium Chloride Solutions ◽  
Plasma Cortisol Concentration

SUMMARY Plasma cortisol concentrations, measured by competitive protein-binding, were examined in intact and hypophysectomized goldfish (Carassius auratus L.) adapted to fresh water or to 210 mm-sodium chloride solutions. The mean plasma cortisol concentration of freshwater-adapted fish (6·6 ± 1·8 (s.e.m.) μg/100 ml plasma) increased after stress and intraperitoneal injections of mammalian corticotrophin. Hypophysectomy resulted in a reduction in plasma cortisol concentration to about 2 μg/100 ml plasma. Transfer of fish to sodium chloride solutions caused rapid, but transitory increases in the plasma cortisol concentrations in intact, but not in hypophysectomized fish. After 3 days in the sodium chloride solution the cortisol levels were similar to those of control fish kept in fresh water. The plasma concentrations of this corticosteroid in goldfish appear to be unrelated to external salinity, although a 'mineralocorticoid' action of the hormone cannot be excluded.

ADRENOCORTICAL FUNCTION TESTS IN DOGS WITH HYPERFUNCTIONING ADRENOCORTICAL TUMOURS

1979 ◽  
Vol 80 (3) ◽  
pp. 315-319 ◽  
Author(s):  
J. C. MEIJER ◽  
A. A. M. E. LUBBERINK ◽  
A. RIJNBERK ◽  
R. J. M. CROUGHS
Keyword(s):  
Plasma Concentration ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Adrenocortical Function ◽  
Plasma Cortisol Concentration ◽  
Function Tests ◽  
Lysine Vasopressin ◽  
Adrenocortical Tumours ◽  
Adrenocortical Tumour

The response has been studied in nine dogs with hyperadrenocorticism due to adrenocortical tumours to the administration of dexamethasone, insulin, lysine-vasopressin and tetracosactide by measuring the changes in plasma cortisol concentration. Administration of dexamethasone did not produce a decrease in the plasma concentration of cortisol in any of these dogs. Administration of insulin caused slight increases in the plasma concentration of cortisol in four out of eight dogs. Lysine-vasopressin increased the plasma concentration of cortisol in eight out of nine dogs, three responded supranormally. Eight out of the nine dogs responded to tetracosactide administration, three responded supranormally. It is concluded that in the dog, in contrast to man, the lysine-vasopressin test cannot be used to differentiate between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to an adrenocortical tumour. Apparently pituitary ACTH is not completely depleted in dogs with hyperfunctioning adrenocortical tumours.

Personality, Physique and the Adrenocortical Response to a Psychological Stress

1967 ◽  
Vol 113 (499) ◽  
pp. 601-605 ◽  
Author(s):  
P. K. Bridges ◽  
M. T. Jones
Keyword(s):  
Psychological Stress ◽  
Emotional Response ◽  
Plasma Cortisol ◽  
Cortisol Concentration ◽  
Urinary Catecholamine ◽  
Catecholamine Excretion ◽  
Plasma Cortisol Concentration ◽  
Adrenocortical Response

There have been a number of studies attempting to quantify anxiety under stress, using biochemical measures such as plasma Cortisol concentration and urinary catecholamine excretion as concomitants of the emotional response. A limitation of some of this work has been the lack of predictable and adequate stresses studied, which have included disturbing interviews (Bliss et al., 1956), admission to hospital and anticipation of operation (Mason, 1959), stressful films (Levi, 1965) and hypnotically induced anxiety (Persky et at., 1959).

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