Abstract:We evaluated the possibility that there is enhanced conversion of Cortisol (F) to cortisone (E) in obese children. IC-Ε was measured from 15 lean children aged 12.7±2.2 years, body mass index Z-score (BMI-SD) = -0.35±0.82, IC-F = 197±70 nM/1 and 9 obese children aged 12.3±3.2 years, BMI-SD = +4.7±2.1, IC-F = 149±53 nM/1. IC-E was higher in lean children 76±25 nM/1 compared to obese 60±11 nM/1 (p<0.04). There was no difference in the ratio of IC-E/IC-F between lean 0.40±0.10 and obese subjects 0.42±0.09 (p<0.6)… Show more
“…In our study, we did not find a significant relationship between waist circumference and cortisol or cortisone. Additionally, we neither found significant differences of cortisol to cortisone ratios between normal-weight children and obese children nor significant changes of this ratio after weight loss according to another study of obese prepubertal children (34). On the other hand, the higher glucocorticoid levels in obesity may also be cause of insulin resistance in obese prepubertal children.…”
In obese prepubertal children, the increased androgens, mineralocorticoid precursors, and glucocorticoids were responsive to weight loss in contrast to DHEAS, suggesting that DHEAS does not seem to be regulated by changes in body mass index.
“…In our study, we did not find a significant relationship between waist circumference and cortisol or cortisone. Additionally, we neither found significant differences of cortisol to cortisone ratios between normal-weight children and obese children nor significant changes of this ratio after weight loss according to another study of obese prepubertal children (34). On the other hand, the higher glucocorticoid levels in obesity may also be cause of insulin resistance in obese prepubertal children.…”
In obese prepubertal children, the increased androgens, mineralocorticoid precursors, and glucocorticoids were responsive to weight loss in contrast to DHEAS, suggesting that DHEAS does not seem to be regulated by changes in body mass index.
“…)0–18Surplus serumImmunoassayNo gender differences1Karbasy (2015) [48]711 (? )0–19?ImmunoassayNo gender differences1Fadalti (1999) [43]82 (49%)6–18Morning sampleImmunoassayNo gender differences0Barra (2015) [49]120 (45%)12.4 ± 3Morning sampleImmunoassayNo gender differences1Chalew (1997) [50]15 (73%)12.7 ± 2.224-h blood withdrawalImmunoassayNo gender differences1Linder (1990) [51]82 (58%)8–1724-h blood withdrawalHPLNo gender differences.0Urine <8 years–Urine 8–18 yearsDorn (1996) [52]20 (55%)15.2 ± 1.124-h urine sampleImmunoassayNo gender differences1
a Number of high risks of bias out of four bias categories (selection, performance, detection, and other biases)Fig. 2Risk of bias graph presenting a summary of the judgements of the accessors concerning risk of bias across all studies included in the meta-analysis.…”
BackgroundGender-specific differences in hypothalamus–pituitary–adrenal (HPA) axis activity have been postulated to emerge during puberty. We conducted a systematic review and meta-analysis to test the hypothesis that gender-specific differences in HPA axis activity are already present in childhood.MethodsFrom inception to January 2016, PubMed and EMBASE.com were searched for studies that assessed non-stimulated cortisol in serum or saliva or cortisol in 24-h urine in healthy males and females aged ≤18 years. Studies that conform with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement were reported. Standardized mean differences (95% CIs) were calculated and analyzed using fixed-effect meta-analysis stratified for age: <8 years (prepubertal) and 8–18 years (peri-/postpubertal). For comparison, we ran the same analyses using random-effects models.ResultsTwo independent assessors selected 413 out of 6158 records (7%) for full-text screening, of which 79 articles were included. Of these, 58 (with data on 16,551 subjects) were included in the meta-analysis. Gender differences in cortisol metabolism differed per age group. Boys aged <8 years had 0.18 (0.06; 0.30) nmol/L higher serum and 0.21 (0.05; 0.37) nmol/L higher salivary cortisol levels, while between 8 and 18 years, boys had 0.34 (0.28; 0.40) nmol/L lower serum and 0.42 (0.38; 0.47) nmol/L lower salivary cortisol levels. In 24-h urine, cortisol was consistently higher in boys, being 0.34 (0.05; 0.64) and 0.32 (0.17; 0.47) μg/24 h higher in the <8- and 8–18-year groups, respectively. However, gender-differences in serum cortisol <8 years and between 8 and 18 years were absent when using random-effects models.ConclusionsGender differences in cortisol metabolism are already present in childhood, with higher salivary cortisol in boys aged <8 years compared to girls. This pattern was reversed after the age of 8 years. In contrast, the gender-specific difference in cortisol production as assessed through 24-h urine did not change with age. Although differences were small, and analyses of gender differences in serum cortisol were inconclusive, they might contribute to gender-specific origins of health and disease.Electronic supplementary materialThe online version of this article (doi:10.1186/s13293-016-0123-5) contains supplementary material, which is available to authorized users.
“…A normal suppression of the HPA axis in response to dexamethasone administration in obesity is supported by numerous studies [5,18,[21][22][23][24], with only few exceptions [25]. Previous findings which also argue against an overactivity of the HPA axis in obesity are the subnormal 24-h mean cortisol plasma concentrations in obese children [26,27] and in obese adults [12,25].…”
Section: Activity Of the Hypothalamic-pituitary-adrenal Axis In Obesitymentioning
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