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, Daniel Macouzet Iturbe, and Francisco Pérez Eugenio from the Computer Unit, IFC, UNAM. References 1 Deng H Jasper H . Sexual dimorphism: how female cells win the race . Current Biology 2016 26 R212 – R21 5 . ( https://doi.org/10
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Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK
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differences ( 5 , 6 , 7 , 8 , 9 , 10 ). Sexual dimorphism in HPA-axis activity has been suggested to be already present in early childhood. A recent meta-analysis suggested that boys and girls differed in basal HPA-axis activity, as assessed by salivary
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Introduction Sexual dimorphisms of some dozen or more hormone- and drug-metabolizing constituent cytochromes P450 (CYPs) observed in rats, humans, and many other species examined ( 1 ) are defined by two characteristics. (i) Following puberty
Department of Pediatrics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Reproduction & Development Research Institute, de Boelelaan, Amsterdam, The Netherlands
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Department of Pediatrics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Reproduction & Development Research Institute, de Boelelaan, Amsterdam, The Netherlands
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Department of Pediatrics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Reproduction & Development Research Institute, de Boelelaan, Amsterdam, The Netherlands
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Objective
Sex-specific differences in hypothalamic–pituitary–adrenal axis activity might explain why male preterm infants are at higher risk of neonatal mortality and morbidity than their female counterparts. We examined whether male and female preterm infants differed in cortisol production and metabolism at 10 days post-partum.
Design and methods
This prospective study included 36 preterm born infants (18 boys) with a very low birth weight (VLBW) (<1.500 g). At 10 days postnatal age, urine was collected over a 4- to 6-h period. Glucocorticoid metabolites were measured using gas chromatography-mass spectrometry. Main outcome measures were: (1) cortisol excretion rate, (2) sum of all glucocorticoid metabolites, as an index of corticosteroid excretion rate, and (3) ratio of 11-OH/11-OXO metabolites, as an estimate of 11B-hydroxysteroid dehydrogenase (11B-HSD) activity. Differences between sexes, including interaction with Score of Neonatal Acute Physiology Perinatal Extension-II (SNAPPE II), sepsis and bronchopulmonary dysplasia (BPD), were assessed.
Results
No differences between sexes were found for cortisol excretion rate, corticosteroid excretion rate or 11B-HSD activity. Interaction was observed between: sex and SNAPPE II score on 11B-HSD activity (P = 0.04) and sex and BPD on cortisol excretion rate (P = 0.04).
Conclusion
This study did not provide evidence for sex-specific differences in adrenocortical function in preterm VLBW infants on a group level. However, in an interaction model, sex differences became manifest under stressful circumstances. These patterns might provide clues for the male disadvantage in neonatal mortality and morbidity following preterm birth. However, due to the small sample size, the data should be seen as hypothesis generating.
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comparable body condition, suggesting that there may be some sexual dimorphism in the roles it plays and possibly the tissues it targets. In women, leptin circulates at much higher concentrations with reports ranging from 40 to 300% higher than that found in
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Introduction The sexual dimorphism in the mechanisms involved in the regulation of somatotroph axis is well documented, and it might account for some of the sex differences in growth rate and body composition ( 1 ). Indeed, sex hormones are
Department of Molecular Endocrinology, National Research Institute for Child Health and Development, Setagaya, Tokyo, Japan
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Department of Molecular Endocrinology, National Research Institute for Child Health and Development, Setagaya, Tokyo, Japan
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Research Center for Environment and Developmental Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan
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Research Center for Environment and Developmental Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan
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Department of Molecular Endocrinology, National Research Institute for Child Health and Development, Setagaya, Tokyo, Japan
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of age or later ( 1 , 4 , 5 , 6 ). Thus, sexual dimorphism in blood sex hormone levels is evident in children above 8 years of age. Furthermore, ultra-sensitive hormone assays using liquid chromatography-tandem mass spectrometry (LC-MS/MS) have
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(In this review, we use the term ‘sex’ to refer to biological aspects of male or female development, whereas we use the term ‘gender’ to refer to an individual’s self-reported sense of gender.) differences before puberty, skeletal sexual dimorphism
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have been proposed to account for the remarkable sexual dimorphism of most human autoimmune diseases (46) . The effects of X chromosomal genes (47, 48, 49) , the effects of Y chromosomal genes (50, 51, 52, 53) , fetal microchimerism in mothers (54
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inconsistencies may be related to the sexual dimorphism in kisspeptin expression, its serum concentrations, and the distribution of kisspeptin receptors, which are believed to explain some of the developmental differences between males and females ( 19 , 20