I Huybrechts1, T De Vriendt2, C Breidenassel3, J Rogiers4, B Vanaelst2, M Cuenca-García5, L A Moreno6, M González-Gross3, R Roccaldo7, A Kafatos8, E Clays4, G Bueno6, L Beghin9, M Sjöstrom10, Y Manios11, D Molnár12, P T Pisa13, S De Henauw14. 1. Department of Public Health, Ghent University, Ghent, Belgium; International Agency for Research on Cancer, Dietary Exposure Assessment Group, Lyon, France. Electronic address: inge.huybrechts@ugent.be. 2. Department of Public Health, Ghent University, Ghent, Belgium; Research Foundation Flanders, Brussels, Belgium. 3. ImFINE Research Group, Department of Health and Human Performance, Universidad Politécnica de Madrid, Spain; Department of Human Nutrition, Rheinische Friedrich-Wilhemls Universität, Bonn, Germany. 4. Department of Public Health, Ghent University, Ghent, Belgium. 5. Department of Medical Physiology, School of Medicine, Granada University, Granada, Spain. 6. Growth, Exercise, Nutrition and Development (GENUD) Research Group, School of Health Science (EUCS), University of Zaragoza, Zaragoza, Spain. 7. Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione (INRAN), Roma, Italy. 8. Department of Social Medicine, School of Medicine, Preventive Medicine and Nutrition Clinic, University of Crete, Crete, Greece. 9. Inserm U955, IFR114, Faculty of Medicine, University Lille 2, Lille, France; CIC-9301-CH&U-Inserm of Lille, CHRU de Lille, Lille, France. 10. Unit for Preventive Nutrition, Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden. 11. Department of Nutrition & Dietetics, Harokopio University, Athens, Greece. 12. Department of Pediatrics, Medical Faculty, University of Pécs, Jzsef A 7, Pécs, Hungary. 13. International Agency for Research on Cancer, Dietary Exposure Assessment Group, Lyon, France; MRC/Wits Developmental Pathways for Health Research Unit, Department of Paediatrics, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. 14. Department of Public Health, Ghent University, Ghent, Belgium; University College Ghent Vesalius, Ghent, Belgium.
Abstract
BACKGROUND AND AIMS: Stress is hypothesized to facilitate the development of obesity, whose the foundations are already set during childhood and adolescence. We investigated the relationship between the stress-system, selected mechanisms of energy homeostasis and insulin resistance (IR) in a sample of European adolescents. METHODS AND RESULTS: Within HELENA-CSS, 723 adolescents (12.5-17.5 years) from 10 European cities provided all the necessary data for this study. Fasting blood samples were collected for cortisol, leptin, insulin and glucose analysis. HOMA-IR was calculated from insulin and glucose concentrations. Adolescents' body fat (BF) %, age and duration of exclusive breastfeeding were assessed. For boys and girls separately, the relationship of cortisol with leptin, insulin, glucose and HOMA-IR was examined by computing Pearson correlation coefficients and Hierarchical Linear Models (HLMs), with 'city' as cluster unit, adjusting for age, BF% and duration of exclusive breastfeeding. In boys, Pearson correlation coefficients illustrated positive correlations of cortisol with insulin (r = 0.144; p = 0.013), glucose (r = 0.315; p < 0.001) and HOMA-IR (r = 0.180; p = 0.002), whilst in girls, this positive relationship was observed for leptin (r = 0.147; p = 0.002), insulin (r = 0.095; p = 0.050) and HOMA-IR (r = 0.099; p = 0.041), but not for glucose (r = 0.054; p = 0.265). Observed associations were independent of adolescents' age, BF% and duration of exclusive breastfeeding after computing HLMs. CONCLUSION: This study suggests that the stress-system is positively related to mechanisms of energy homeostasis and IR in European adolescents, and reveals a potential small gender difference in this relationship. The hypothesis that stress might facilitate the development of obesity during adolescence is supported.
BACKGROUND AND AIMS: Stress is hypothesized to facilitate the development of obesity, whose the foundations are already set during childhood and adolescence. We investigated the relationship between the stress-system, selected mechanisms of energy homeostasis and insulin resistance (IR) in a sample of European adolescents. METHODS AND RESULTS: Within HELENA-CSS, 723 adolescents (12.5-17.5 years) from 10 European cities provided all the necessary data for this study. Fasting blood samples were collected for cortisol, leptin, insulin and glucose analysis. HOMA-IR was calculated from insulin and glucose concentrations. Adolescents' body fat (BF) %, age and duration of exclusive breastfeeding were assessed. For boys and girls separately, the relationship of cortisol with leptin, insulin, glucose and HOMA-IR was examined by computing Pearson correlation coefficients and Hierarchical Linear Models (HLMs), with 'city' as cluster unit, adjusting for age, BF% and duration of exclusive breastfeeding. In boys, Pearson correlation coefficients illustrated positive correlations of cortisol with insulin (r = 0.144; p = 0.013), glucose (r = 0.315; p < 0.001) and HOMA-IR (r = 0.180; p = 0.002), whilst in girls, this positive relationship was observed for leptin (r = 0.147; p = 0.002), insulin (r = 0.095; p = 0.050) and HOMA-IR (r = 0.099; p = 0.041), but not for glucose (r = 0.054; p = 0.265). Observed associations were independent of adolescents' age, BF% and duration of exclusive breastfeeding after computing HLMs. CONCLUSION: This study suggests that the stress-system is positively related to mechanisms of energy homeostasis and IR in European adolescents, and reveals a potential small gender difference in this relationship. The hypothesis that stress might facilitate the development of obesity during adolescence is supported.
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