ECE2015 Eposter Presentations Reproduction, endocrine disruptors and signalling (92 abstracts)
1Laboratory of Biology and Physiology of Organisms, Endocrinology Team, Faculty of Biological Sciences, USTHB, Algiers, Algeria; 2Department of Endocrinology, IBN ZIRI Hospital, Bologhine, Algiers, Algeria; 3Laboratory of Biology and Physiology of Organisms, Bioenergetic and Intermediate Metabolism Team, Faculty of biological Sciences, USTHB, Algiers, Algeria.
Introduction: Excess of abdominal fat may disturb metabolic parameters that affect insulin level and may lead to menstrual disorders, consecutively to disturbance in sex steroids production. The aim is to link the metabolic hormones in abdominal obesity, with reproductive axis hormones in women at age.
Patients and methods: 85 no menopausal women aged between 17 and 52 were recruited: 62 with abdominal obesity (BMI >30 kg/m2 and waist circumference >80) and 23 normal weight for controls (BMI <25). Lipidemia, fasting plasma glucose, insulin, leptin, adiponectin, LH, FSH, oestradiol (in follicular phase), progesterone (in luteal phase), 17OHP, SDHEA, total and free testosterone using free androgen index (FAI), and sex hormone binding globulin (SHBG) were analysed. Insulin resistance and sensitivity were estimated by HOMA-IR and QUIKI indexes.
Results: Obese women show ovulation disorders (52%) type spaniomenorrhea sometimes up to amenorrhea, hirsutism (50.79%), acne (25.4%) associated to high leptin (60.91%, P<0.001), cholesterol (17.32%, P=0.00017), triglycerides (38.98%, P=0.00014), LDL-c (18.80%, P=0.0014), decreased HDL-c (17.02%, P=0.0085), and insulin resistance (HOMA: 10.11 vs 4.39) due to decreased insulin sensitivity (QUIKI: 0.68 vs 0.83). The high levels of FSH (32.89%, P=0.0495), oestradiol (11.18%, P=0.46), LH (16.93%, P=0.349), total and free testosterone (15%, P=0.23), and FAI (20.42%), were associated to significant rise of leptin (68.69%, P=0.001), slight decrease of adiponectin reduced both progesterone (64.22%, P=0.0003), 17OHP (24.34%, P=0.18), and DHEAS (8%, P=0.587) as well as circulating SHBG (11.83%, P=0.38).
Conclusion: Insulin resistance and dyslipidaemia in obese women may contribute to increase aromatase activity and decrease liver SHBG production which led to increase total and free plasma testosterone, whereas the rise of plasma gonadotropins should be consecutive to the stimulating effect of leptin on LHRH neurons. According to clinical thresholds, our results may suggest the occurrence of hyperandrogenism in obese women, but not associated with polycystic ovary syndrome.
Disclosure: This work was supported by financial gift from the Algerian National Research Program (PNR).