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Hôpital-Camfrout, France

Maimoun L.,Service dHormonologie | Sultan C.,Service dHormonologie | Sultan C.,Montpellier University
Metabolism: Clinical and Experimental

Physical exercise is recommended to improve bone mass in growing children and decrease bone loss in elderly men and women. However, the specific mechanisms by which exercise influences bone metabolism are still not thoroughly understood. The effect of physical activity on the skeleton is generally evaluated by dual-energy x-ray absorptiometry, which measures bone mineral density. However, a relatively long period is needed to detect even a minor variation in bone mineral density with this technique, limiting its usefulness. Bone biochemical markers that reflect the cellular activities of bone formation and resorption are thus also useful tools, both to monitor the acute effects of exercise on bone remodeling and to investigate the mechanisms of exercise-induced changes in bone mass. This article describes the effects of physical activity on bone remodeling in various types of population. The comparison of sedentary individuals and athletes with many years of high-volume sports practice, for example, has clarified some of the long-term effects of exercise. Moreover, the acute variation in bone cell activities after brief exercise or a training program is here examined. The interpretation of results is difficult, however, because of the many parameters, such as age, that are involved. The various populations are therefore categorized to reflect the biological factors implicated in the modulation of bone marker response during exercise. © 2011 Elsevier Inc. All rights reserved. Source

Maimoun L.,Service dHormonologie | Coste O.,Service dHormonologie | Jaussent A.,Hopital Arnaud de Villeneuve | Mariano-Goulart D.,Service de Medecine Nucleaire | And 2 more authors.
Clinical Endocrinology

Objectives Although hypoleptinaemia has been reported in female peripubertal athletes, data are lacking on leptin and bone mass variations in puberty and the effects of leptin on bone mineralization during this period. This study therefore investigated the variations in leptin level and bone mineral density (BMD) in young elite female rhythmic gymnasts (FRG) according to pubertal stage. The effects of leptin, IGF-1 and sex hormones on bone mineral acquisition were also evaluated. Patients and measurements Plasma leptin levels were analysed in 43 elite FRG (mean age: 13·3 ± 1·8 years range: 10·6-17·2, body mass index: 17·52 ± 1·85 kg/m, training status: 17·9-23·8 h/week) according to their pubertal stage (Tanner I, n = 7; II, n = 10; III, n = 9; IV, n = 8; V, n = 9). IGF-1, IGFBP-3 and sex hormones were also evaluated. BMD was measured by dual-energy X-ray absorptiometry at various bone sites. Results Plasma leptin increased throughout pubertal growth and the values measured in Tanner stages IV-V were significantly higher than in stages I-II. Gains in BMD were measured throughout puberty at all bone sites, particularly between Tanner stages II and IV. In simple correlation analysis, BMD at all bone sites was positively correlated with plasma leptin, age, bone age, BMI, oestrogen, testosterone, IGF-1 and IGFBP-3. However, multivariate analysis using a linear regression model by block (including bone age, anthropometric data and biological parameters) was then performed to determine the factors independently associated with each BMD site, and only bone age, fat-free soft tissue and BMI remained independent predictors. Conclusion In FRG characterized by high training volume and low fat mass, plasma leptin levels increased throughout puberty and were partially related to body composition changes. Despite the simultaneous increases in plasma leptin and BMD during pubertal growth, it was not possible to differentiate the leptin impact on bone independently from anthropometric parameters. © 2010 Blackwell Publishing Ltd. Source

Maimoun L.,Montpellier University | Maimoun L.,French Institute of Health and Medical Research | Guillaume S.,French Institute of Health and Medical Research | Lefebvre P.,Diabete | And 15 more authors.
Journal of Clinical Endocrinology and Metabolism

Background: The nutritional deprivation of adolescent girls with anorexia nervosa (AN) reduces bone mass acquisition. A better understanding of this process would improve the medical treatment of bone alteration and its long-term consequences. Objective: The first aim was to model the bone mass acquisition in young women with AN. The second aimwasto identify the clinical and biological factors associated with boned emineralization and investigate the potential role of sclerostin and dickkopf-1 protein (DKK-1). Population and Methods: Ninety-eight AN patients (mean age 18.2 ± 2.6 years) and 63 agematched controls were enrolled in this study. Areal bone mineral density (aBMD) was determined by dual-energy x-ray absorptiometry. Calciotropic hormones, bone turnover markers, sclerostin, DKK-1, and growth factors were concomitantly evaluated. Results: The aBMD was significantly reduced at all bone sites in AN patients vs controls (range,-3.3% at the radius to -12.1% for total proximal femur). Bone formation markers IGF-1 and DKK-1 were significantly decreased in AN patients, whereas PTH, sclerostin, and the bone resorption markers were increased. In patients, the AN duration, amenorrhea, weight, body mass index, fat mass, and fat-free soft tissue were negatively correlated with a BMD, whereas the age of AN onset was positively correlated. Multiple regression analysis revealed that the duration of amenorrhea was the independent factor most negatively associated with a BMD at all bone sites except the radius. Conclusion: This case-control study demonstrated a dramatic reduction in a BMD, reinforced for the first time by our models, and indicates the need for early, systematic, and adapted bone mass monitoring. Moreover, appropriate treatment should be started early in patients with AN. Increased secretion of sclerostin suggests that it may be a target for pharmacological action. Copyright © 2014 by the Endocrine Society. Source

Maimoun L.,Service dHormonologie | Philibert P.,Service dHormonologie | Bouchard P.,Service dendocrinologie | Ocal G.,Ankara University | And 5 more authors.
Fertility and Sterility

Objective: To determine the genetic cause of primary amenorrhea. Design: Case series. Setting: Pediatric endocrinology, endocrinology, and gynecology departments of academic hospitals. Patient(s): Three adolescents and one young woman 46, XY patients with srd5A2 gene mutations. Main Outcome Measure(s): Genetic analysis of srd5A2. Result(s): We report four srd5A2 gene mutations in three adolescents and one young woman with 46,XY primary amenorrhea. All presented clitoromegaly and two presented hypospadias; all had been reared as females. Virilization of the external genitalia was noted in the pubertal period in all four patients. Three were maintained in the female sex of rearing by personal choice, and the fourth switched gender. We identified the homozygous substitutions p.L55Q (exon 1), p.Q56R (exon 1), and p.N193S (exon 4), in patients 1, 2, and 3, respectively. Patient 4 had compound heterozygous mutations, a new c.34delG (exon 1) associated with p.R246W (exon 5). All patients had high plasma T levels (ranges, 16.2-23.2 nmol/L; normal female teenage range, 0.35-2 nmol/L). Conclusion(s): Our data clearly demonstrate that 5α-reductase deficiency should be considered in XY adolescents with primary amenorrhea and no breast development associated with virilization at puberty and high plasma T. Positive parental consanguinity should reinforce the diagnostic orientation. © 2011 American Society for Reproductive Medicine, Published by Elsevier Inc. Source

Morel Y.,Service dHormonologie | Roucher F.,Service dHormonologie | Plotton I.,Service dHormonologie | Goursaud C.,Service dHormonologie | And 2 more authors.
Annales d'Endocrinologie

Progesterone, estrogens, androgens and glucocorticoids are involved in pregnancy from implantation to parturition. Their biosynthesis and their metabolism result from complex pathways involving the fetus, the placenta and the mother. The absence of expression of some steroïdogenic enzymes as CYP17 in placenta and in adrenal fetal zone and the better determination of the onset and variation of others especially HSD3B2 during the pregnancy explain the production of the steroid hormones. Moreover the consequences of some disorders of steroidogenesis (especially aromatase, POR, CYP11A1 and 21-hydroxylase deficiencies) in fetus and mother during the pregnancy have permit to elucidate these complex pathways. This better knowledge of steroid hormones production associated with their dosages in maternal plasma/urine or amniotic fluid using new specific assays as LC-MS MS could facilitate the follow-up of normal and pathological pregnancies. Moreover, these advances should be a basis to evaluate the impact of multiple pathologies of the pregnancy and pharmacologic and xenobiotic consequences on their metabolism. © 2016 Elsevier Masson SAS. Source

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