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Cortisol Production (cortisol + production)

Distribution by Scientific Domains

Medical Sciences	72%

Selected Abstracts

Decreased cortisol production in male type 1 diabetic patients

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2003
M. N. Kerstens
Abstract Background It is unclear whether cortisol production and the 11,HSD-mediated cortisol to cortisone interconversion are different between type 1 diabetic patients and healthy subjects. Materials and methods Fourteen male, nonobese, normotensive type 1 diabetic patients without severe complications (HbA1c < 8·5%) were studied twice during a daily sodium intake of 50 and 200 mmol, and were then compared with 14 individually matched healthy subjects. Cortisol production was assessed by the sum of urinary cortisol metabolite excretion. Urinary ratios of (tetrahydrocortisol + allo-tetrahydrocortisol)/tetrahydro-cortisone [(THF + allo-THF)/THE] and of free cortisol/free cortisone [UFF/UFE] were determined as parameters of 11,HSD activity. Results Sum of urinary cortisol metabolite excretion during low- and high-salt diet was 7·4 ± 2·5 vs. 7·7 ± 2·3 nmol min,1 m,2 (NS) in diabetic patients and 9·7 ± 2·1 vs. 11·2 ± 4·1 nmol min,1 m,2 (NS) in healthy subjects, respectively (P < 0·05 vs. healthy subjects at both diets). The allo-THF excretion and allo-THF/THF ratios were lower in the diabetic than in the healthy males during both diets (P < 0·05). Urinary (THF + alloTHF)/THE and UFF/UFE were similar in both groups and remained unchanged after salt loading. Conclusions The sum of urinary cortisol metabolite excretion as a measure of cortisol production is lower in nonobese, normotensive type 1 diabetic males with adequate glycaemic control and without severe complications, irrespective of sodium intake. We suggest that this is at least in part as result of diminished 5, reductase activity, resulting in a decreased cortisol metabolic clearance. In type 1 diabetic and in healthy males, the 11,HSD setpoint is not affected by physiological variations in sodium intake. [source]

Developmental changes in baseline cortisol activity in early childhood: Relations with napping and effortful control

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2004
Sarah E. Watamura
Abstract Development of the hypothalamic,pituitary,adrenocortical (HPA) axis was examined using salivary cortisol levels assessed at wake-up, midmorning, midafternoon, and bedtime in 77 children aged 12, 18, 24, 30, and 36 months, in a cross-sectional design. Hierarchical linear modeling (HLM) analyses were used to characterize cortisol production across the day and to examine age-related differences. Using area(s) under the curve (AUC), cortisol levels were higher among the 12-, 18-, and 24-month children than among the 30- and 36-month children. For all five age groups, cortisol levels were highest at wake-up and lowest at bedtime. Significant decreases were noted between wake-up and midmorning, and between midafternoon and bedtime. Unlike adults, midafternoon cortisol levels were not significantly lower than midmorning levels. Over this age period, children napped less and scored increasingly higher on parent reports of effortful control. Among the 30- and 36-month children, shorter naps were associated with more adultlike decreases in cortisol levels from midmorning to midafternoon. Considering all of the age groups together, effortful control correlated negatively with cortisol levels after controlling for age. These results suggest that circadian regulation of the HPA axis continues to mature into the third year in humans, and that its maturation corresponds to aspects of behavioral development. © 2004 Wiley Periodicals, Inc. Dev Psychobiol 45: 125-133, 2004. [source]

The relationship between melatonin and cortisol rhythms: clinical implications of melatonin therapy

DRUG DEVELOPMENT RESEARCH, Issue 3 2005
N. Zisapel
Abstract Disturbances in circadian rhythm have been linked to chronic diseases such as insomnia, hypertension, diabetes, and depression. Here we review recent studies on the age-related changes in cortisol and melatonin rhythms and then present descriptive statistics on our preliminary findings on the rectification of the cortisol rhythms by melatonin therapy in elderly patients with insomnia. In adults, the melatonin onset typically occurs during low cortisol secretion. Administration of exogenous melatonin around dusk will shift the phase of the human circadian clock to earlier hours (advance phase shift) leading to phase advances in circadian rhythms (e.g., sleep, endogenous melatonin, cortisol). With aging, the production of melatonin declines and is shifted to later hours while the production of cortisol increases and its peak occurs earlier in the night. In a randomized placebo-controlled crossover study with 8 patients with insomnia aged 55 years and older, a group characterized by low and delayed melatonin production, administration of prolonged-release melatonin in the evening was able to rectify the early onset cortisol production. This delay in nocturnal cortisol onset may explain in part the improvement in sleep quality in elderly patients with insomnia, in schizophrenics, and in depressed patients. Support of circadian pacemaker function by melatonin may provide a new strategy in the treatment of disorders related to impairments in the internal temporal order. The clinical benefit from a decrease in cortisol during the early part of the night may lie beyond the improvement of sleep into a better control of blood pressure, metabolism, and mood. Drug Dev. Res. 65:119,125, 2005. © 2005 Wiley-Liss, Inc. [source]

Decreased cortisol production in male type 1 diabetic patients

The adrenal cortex and steroidogenesis as cellular and molecular targets for toxicity: critical omissions from regulatory endocrine disrupter screening strategies for human health?

JOURNAL OF APPLIED TOXICOLOGY, Issue 2 2003
Philip W. Harvey
Abstract Current testing strategies to assess the endocrine disrupting properties of chemicals have omitted examination of the adrenal gland and do not adequately cover the process of steroidogenesis. Steroidogenesis is critical for adrenocortical function as well as that of the testes and ovaries, and presents multiple molecular targets for toxicity, ranging from general effects on all steroidogenic tissues (e.g. via StAR protein or CYP11A1 cholesterol side-chain cleavage) through to speci,c targets affecting only adrenocortical function (e.g. CYP11,/18 and glucocorticoid synthesis). Numerous chemicals of environmental relevance are now being shown to affect adrenocortical function both in vivo in aquatic species and in vitro in human cell lines, and given the vital role of the adrenal gland to human health and development, there is a strong case for including dedicated assessment techniques in screening batteries for endocrine-disrupting chemicals, not least to assist in general data interpretation (e.g. whether adrenal hypertrophy is due to stress or to a more sinister adrenocortical insuf,ciency). Cell lines such as H295R (derived from a human adrenocortical adenocarcinoma) currently exist that will allow assessment of cortisol production and most of the major enzymes and functional proteins in the steroidogenic pathway (e.g. StAR; CYP11A1/scc; CYP11,/18; CYP17; CYP19; CYP21; 3, -hydroxysteroid dehydrogenase). Adequate assessment of adrenocortical function, as with any component of the integrated endocrine system, probably also will require the development of speci,c in vivo methodology to include effects on hypothalamo-pituitary function. Finally, although there is currently no direct evidence that environmental exposure to endocrine-disrupting (oestrogenic) chemicals has actually caused adverse human health effects, lessons have been learned on their potential from the diethylstilboestrol case. Similar evidence exists from aminoglutethimide and etomidate on the lethal impact of unpredicted chemically induced adrenal insuf,ciency in sensitive human subgroups, and it would seem prudent to incorporate relevant tests for adrenal function and steroidogenesis into current regulatory validation programmes. Published in 2003 by John Wiley & Sons, Ltd. [source]

Psychological trauma associated with the World Trade Center attacks and its effect on pregnancy outcome

PAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 5 2005
Stephanie Mulherin Engel
Summary The destruction of the World Trade Center (WTC) on 11 September 2001 was a source of enormous psychological trauma that may have consequences for the health of pregnant women and their fetuses. In this report, we describe the impact of extreme trauma on the birth outcomes of women highly exposed to the WTC. We enrolled 187 women who were pregnant and living or working within close proximity to the WTC on 11 September. Among women with singleton pregnancies, 52 completed at least one psychological assessment prior to delivery. In adjusted multivariable models, both post-traumatic stress symptomatology (PTSS) and moderate depression were associated with longer gestational durations, although only PTSS was associated with decrements in infant head circumference at birth (, = ,0.07, SE = 0.03, P = 0.01). The impact of stress resulting from extreme trauma may be different from that which results from ordinary life experiences, particularly with respect to cortisol production. As prenatal PTSS was associated with decrements in head circumference, this may influence subsequent neurocognitive development. Long-term follow-up of infants exposed to extreme trauma in utero is needed to evaluate the persistence of these effects. [source]

HPA axis safety of fluticasone furoate nasal spray once daily in children with perennial allergic rhinitis

PEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 3 2009
Ita Tripathy
The effects of intranasal corticosteroids (INSs) on the hypothalamic,pituitary,adrenal (HPA) axis should be assessed for any to be marketed INS. The objective of this study was to assess the effects of fluticasone furoate nasal spray (FFNS) on cortisol production (as a measure of HPA axis function) following 6 wk of treatment with FFNS 110 ,g once daily (QD) compared with placebo in pediatric patients with perennial allergic rhinitis (PAR). In this double-blind, parallel-group study, patients (n = 112) aged 2,11 yr with a 1-yr history of PAR (6 months for patients aged 2,3 yr) were randomized in a 1:1 ratio to either placebo or FFNS. Serum cortisol (SC) concentrations and urinary cortisol (UC) excretion were measured over a 24-h period at the randomization (baseline) and final treatment (week 6) visits for HPA axis evaluation in a domiciled environment (overnight in the clinic). Plasma samples were collected for FFNS at several time points over the 24 h after the final dose for pharmacokinetic analyses. FFNS was non-inferior to placebo with respect to change from baseline (expressed as a ratio) in 24-h SC weighted mean. The lower limit of the two-sided 95% confidence interval (CI) for the treatment ratio was greater than the pre-specified non-inferiority margin of 0.8 (treatment ratio = 0.97, 95% CI 0.88,1.07). UC excretion over 24 h at baseline and end of treatment was similar between treatment groups; no patients had 24-h excretion levels below normal range after 6 wk of treatment. Plasma concentrations of FFNS were generally non-quantifiable (<10 pg/ml). Results of the current study indicate that FFNS 110 ,g QD has no significant effect on HPA axis function in 2- to 11-yr-old pediatric patients with PAR. [source]

Pattern of maternal circulating CRH in laboratory-housed squirrel and owl monkeys

AMERICAN JOURNAL OF PRIMATOLOGY, Issue 11 2010
M.L. Power
Abstract The anthropoid primate placenta appears to be unique in producing corticotropin-releasing hormone (CRH). Placental CRH is involved in an endocrine circuit key to the production of estrogens during pregnancy. CRH induces cortisol production by the maternal and fetal adrenal glands, leading to further placental CRH production. CRH also stimulates the fetal adrenal glands to produce dehydroepiandrostendione sulfate (DHEAS), which the placenta converts into estrogens. There are at least two patterns of maternal circulating CRH across gestation among anthropoids. Monkeys examined to date (Papio and Callithrix) have an early-to-mid gestational peak of circulating CRH, followed by a steady decline to a plateau level, with a possible rise near parturition. In contrast, humans and great apes have an exponential rise in circulating CRH peaking at parturition. To further document and compare patterns of maternal circulating CRH in anthropoid primates, we collected monthly blood samples from 14 squirrel monkeys (Saimiri boliviensis) and ten owl monkeys (Aotus nancymaae) during pregnancy. CRH immunoreactivity was measured from extracted plasma by using solid-phase radioimmunoassay. Both squirrel and owl monkeys displayed a mid-gestational peak in circulating CRH: days 45,65 of the 152-day gestation for squirrel monkeys (mean±SEM CRH=2,694±276,pg/ml) and days 60,80 of the 133-day gestation for owl monkeys (9,871±974,pg/ml). In squirrel monkeys, circulating CRH declined to 36% of mean peak value by 2 weeks before parturition and then appeared to increase; the best model for circulating CRH over gestation in squirrel monkeys was a cubic function, similar to previous results for baboons and marmosets. In owl monkeys, circulating CRH appeared to reach plateau with no subsequent significant decline approaching parturition, although a cubic function was the best fit. This study provides additional evidence for a mid-gestational peak of maternal circulating CRH in ancestral anthropoids that has been lost in the hominoid lineage. Am. J. Primatol. 72:1004,1012, 2010. © 2010 Wiley-Liss, Inc. [source]

Endogenous glucocorticoids and antigen-induced acute and late phase pulmonary responses

CLINICAL & EXPERIMENTAL ALLERGY, Issue 9 2000
Stokes Peebles
Background Several studies suggest that endogenous glucocorticoids can dampen the severity of experimental allergic reactions in animals. Objective To investigate the influence that endogenous glucocorticoids have on the course of IgE-mediated pulmonary early and late phase reactions. Methods Twenty-one allergic asthmatic and six healthy control subjects underwent inhaled antigen challenge with measurements of plasma cortisol and cortisone by gas chromatography-mass spectrometry. Results There were no differences between the asthmatic and control groups in the baseline levels of cortisol or cortisone. However, the asthmatic subjects had significantly higher cortisol levels (67.2 ± 8.6 vs 35.1 ± 4.5 ng/mL; P = 0.04) and had higher cortisol/cortisone ratios (4.8 ± 0.6 vs 3.0 ± 0.2; P = 0.01) 8 h after challenge compared to the control subjects. Among the asthmatic subjects, those whose FEV1 recovered rapidly had higher baseline levels of cortisol and those who displayed a late phase reaction had lower levels of cortisol during the late phase period. Conclusion The results suggest that endogenous glucocorticoids may play a significant role in the modulation of airway responses to antigen challenge, and that antigen challenge may induce cortisol production in allergic subjects. [source]

Profile, mean residence time of ACTH and cortisol responses after low and standard ACTH tests in healthy volunteers

CLINICAL ENDOCRINOLOGY, Issue 3 2006
P. Alía
Objective, No consensus exists until now about the suitable dose of tetracosactin in the ACTH stimulation test for detecting adrenal insufficiency. Our aim was to characterize both the ACTH(1,24) and the cortisol profiles after standard high-dose test (250 µg) (HDT) and low-dose test (1 µg) (LDT) in healthy subjects in order to provide a deeper knowledge about the relationship between stimulus and response. Design and patients, ACTH tests were performed in 10 healthy volunteers (five men, five women) with at least 1 week of difference. Measurements, Plasma ACTH(1,24) and ACTH(1,39) and serum cortisol were measured before tetracosactin i.v. injection and at 5, 15, 30, 45, 60, 75 and 90 min after stimulus. Area under the curve (AUC) of ACTH(1,24) and cortisol, as well as mean residence time (MRT) for ACTH(1,24) were calculated in both tests. Results, Elimination of ACTH(1,24) was faster in HDT than in LDT (MRTs of 0·14 vs 0·37, respectively, P = 0·008), but plasma concentrations were higher up to 60 min cortisol production in HDT reaching a higher maximum concentration (Cmax: 1144 vs 960 nmol/l) but delayed in time (75 vs 52·5 min). No significant relationship was observed between AUC or Cmax of ACTH(1,24) and AUC, Cmax and increment of cortisol in any of the tests. However, a negative correlation of basal cortisol values was observed with relative cortisol increment (HDT: r = 0·77 P = 0·009; LDT: r = 0·94 P < 0·0001), but not so with Cmax (HDT: r = 0·22 P = 0·55; LDT: r = 0·57 P = 0·09). Conclusions, The elimination rate of ACTH in healthy volunteers was significantly lower in LDT than in HDT, but cortisol production rate appears to be identical in both tests, so that a maximum adrenal stimulation seems to exist. The use of LDT may be more adequate, although data from patients need studying. [source]