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      Increased Cortisol and Cortisone Levels in Overweight Children

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          Abstract

          Background

          It has been unclear whether relatively high cortisol and cortisone levels are related to overweight in childhood, parental body mass index (BMI), and family dietary habits. The aim of this study was to compare cortisol and cortisone levels in urine and saliva from overweight and normal children, as well as correlations between children’s BMI, parental BMI and family dietary behavior questionnaire score (QS).

          Material/Methods

          We analyzed the data from 52 overweight children and 53 age- and sex-matched normal-weight children aged 4–5 years. The concentrations of salivary cortisol (SF), salivary cortisone (SE), urinary cortisol (UF) and urinary cortisone (UE) were measured using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). The family dietary behavior QS was answered by the parent mainly responsible for the family diet.

          Results

          Average cortisol and cortisone levels were significantly higher in overweight children. There was no significant difference in the ratio of cortisol to cortisone ( R cc ) and the marker of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) activities. The results displayed correlations among cortisol, cortisone, and R cc . Positive correlations were weak-to-moderate between BMI and SF, SE, UF, and UE. There were correlations between BMI and maternal BMI (mBMI), and BMI was significantly associated with QS.

          Conclusions

          Our results suggest that cortisol and cortisone levels are associated with overweight in children, but the 11β-HSD2 activities showed no significant differences. Unhealthy family diet was associated with higher BMI, UF, and UE, and families with maternal overweight or obesity had a higher prevalence of children’s overweight or obesity.

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          Most cited references34

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          Development of adiposity in adolescence: five year longitudinal study of an ethnically and socioeconomically diverse sample of young people in Britain.

          To examine the developmental trajectory of obesity in adolescence in relation to sex, ethnicity, and socioeconomic status. Five year longitudinal cohort study of a socioeconomically and ethnically diverse sample of school students aged 11-12 years at baseline. 36 London schools recruited to the study in 1999 by a stratified random sampling procedure. 5863 students participated in one or more years. Weight, height, and waist circumference measured annually by trained researchers; overweight and obesity defined according to International Obesity Task Force criteria; adiposity and central adiposity indexed by body mass index (BMI) and waist standard deviation scores relative to 1990 British reference values. In school year 7 (age 11-12), the prevalence of overweight and obesity combined was almost 25%, with higher rates in girls (29%) and students from lower socioeconomic backgrounds (31%) and the highest rates in black girls (38%). Prevalence of obesity increased over the five years of the study at the expense of overweight, but no reduction occurred in the proportion of students with BMIs in the healthy range. Waist circumferences were high compared with 1990 norms at age 11 (by 0.79 SD in boys and by 1.15 SD in girls) and increased further over time. Both BMI and waist circumference tracked strongly over the five years. Prevalence of overweight and obesity was high in London school students, with significant socioeconomic and ethnic inequalities. Little evidence was found of new cases of overweight or obesity emerging over adolescence, but few obese or overweight adolescents reduced to a healthy weight. The results indicate that persistent obesity is established before age 11 and highlight the need to target efforts to prevent obesity in the early years.
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            Impact of parental BMI on the manifestation of overweight 5-7 year old children.

            There is an increase in the prevalence of overweight and obese children. Genetic and environmental factors are contributing factors but the influence of parental nutritional state on early manifestation of overweight is not well characterised. To systematically investigate the impact of parental BMI on the manifestation of overweight in 5 to 7 year old children. Cross-sectional study (as a part of the Kiel Obesity Prevention Study [KOPS]) of 3306 children aged 5-7 years and their parents. The nutritional state of the children (BMI, triceps skinfold, fat mass, prevalence of overweight) was investigated in subgroups differing with respect to parental BMI. BMI of the children was significantly correlated with parental BMI (r = 0.272, p < 0.01). Children's BMI showed closer associations with maternal than with paternal BMI (r = 0.254 vs. 0.159, p < 0.01). A multivariate regression analysis showed that parental BMI explained 7.6 % of the variance in children's BMI. OR for overweight was elevated in children with at least one overweight parent (overweight mother: OR 2.9 (boys)/3.1 (girls); overweight father: OR 1.8 (boys)/2.4 (girls). OR was highest for children with two obese parents (OR 7.6 (boys)/6.3 (girls). Children with one obese parent were more frequently overweight than children with one overweight parent. Parental BMI showed only a weak correlation with the BMI of their children. However, children's risk of becoming overweight increased with parental overweight and obesity. Thus, familial disposition has to be taken into account to identify risk groups for preventive measures.
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              Stress, visceral obesity, and metabolic complications.

              Stress is a state of threatened homeostasis or disharmony caused by intrinsic or extrinsic adverse forces and is counteracted by an intricate repertoire of physiologic and behavioral responses that aim to reestablish the challenged body equilibrium. The adaptive stress response depends upon an elaborate neuroendocrine, cellular, and molecular infrastructure, the stress system. Crucial functions of the stress system response are mediated by the hypothalamic-pituitary-adrenal (HPA) axis and the central and peripheral components of the autonomic nervous system (ANS). The integrity of the HPA axis and the ANS and their precise interactions with other CNS components are essential for a successful response to the various stressors. Chronic stress represents a prolonged threat to homeostasis by persistent or frequently repeated stressors and may lead to manifestations that characterize a wide range of diseases and syndromes. Such states progressively lead to a deleterious overload with complications caused by both the persistent stressor and the detrimental prolongation of the adaptive response. The metabolic syndrome can be described as a state of deranged metabolic homeostasis characterized by the combination of central obesity, insulin resistance, dyslipidemia, and hypertension. The incidence of both obesity and the metabolic syndrome in modern Western societies has taken epidemic proportions over the past decades and often correlates with indices of stress in the affected populations. Stress, primarily through hyperactivation of the HPA axis, appears to contribute to the accumulation of fat tissue, and vice versa, obesity itself seems to constitute a chronic stressful state and may cause HPA axis dysfunction. In addition, the description of obesity as a systemic low grade inflammatory condition that contributes to the derangement of the metabolic equilibrium implies that the proinflammatory cytokines which are secreted by the adipocytes hold a potentially important pathogenetic role. In this article we describe the physiology of the stress system response, with emphasis on metabolism, and review the recent data that implicate several neuroendocrine and inflammatory mechanisms mobilized during chronic stress in the development of the metabolic complications that characterize central obesity and the metabolic syndrome.
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                Author and article information

                Journal
                Med Sci Monit Basic Res
                Med Sci Monit Basic Res
                Medical Science Monitor Basic Research
                Medical Science Monitor Basic Research
                International Scientific Literature, Inc.
                2325-4394
                2325-4416
                2017
                09 February 2017
                : 23
                : 25-30
                Affiliations
                [1 ]Key Laboratory of Environmental Medicine and Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu, P.R. China
                [2 ]Key Laboratory of Child Development and Learning Science of Ministry of Education, Research Centre for Learning Science, Southeast University, Nanjing, Jiangsu, P.R. China
                [3 ]Division of Child Care, Suzhou Municipal Hospital, Suzhou, Jiangsu, P.R. China
                Author notes
                Corresponding Authors: Xuejun Kang, e-mail: xjkang64@ 123456163.com , Yuan Song, e-mail: Yuanyuan-sy@ 123456163.com
                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                [*]

                Xuejun Kang and Yuan Song contributed equally to this work

                Article
                902707
                10.12659/MSMBR.902707
                5314734
                28179618
                2e32a12f-3e9f-48a2-8831-270423315d6e
                © Med Sci Monit, 2017

                This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

                History
                : 05 December 2016
                : 09 January 2017
                Categories
                Human Study

                child,cortisol,cortisone,overweight
                child, cortisol, cortisone, overweight

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