ABSTRACT
Background & objectives: Polycystic Ovary Syndrome (PCOS) is becoming an area of global and national health concern. It requires a life cycle approach from adolescence to menopause. To comprehensively address the wide spectrum of this disorder, a multidisciplinary model of care was established for women with PCOS in a government setting in India with an objective to screen and manage multifaceted manifestations of PCOS and to diagnose and treat associated comorbidities such as metabolic syndrome, dermatologic manifestations and psychological issues. Methods: A model of integrated multidisciplinary PCOS clinic was implemented for services and research at ICMR-National Institute for Research in Reproductive and Child Health (NIRRCH), Mumbai Maharashtra, India. This is a one-stop holistic centre for managing menstrual, cosmetic, infertility, obesity, metabolic and psychological concerns of women affected with PCOS. Two hundred and twenty six women diagnosed with PCOS using the Rotterdam criteria were screened for metabolic comorbidities with anthropometry, ultrasonography, hormonal and biochemical tests and for psychological problems. Analysis was performed using SPSS version 19.0. Results: Mean body mass index (BMI) was 26.1 kg/m2, higher for Asians. Hirsutism was observed in 53.6 per cent of women. Metabolic syndrome was seen among 35.3 per cent and non-alcoholic fatty liver in 18.3 per cent. Psychological issues such as anxiety and depression were identified in majority of the women 31.4 per cent of women could achieve pregnancy at the end of one year of multidisciplinary management. Interpretation & conclusions: The results of the present study suggest that an integrated multidisciplinary approach led to the early identification and treatment of comorbidities of PCOS, especially metabolic syndrome. There is hence an urgent need to implement multidisciplinary PCOS clinics in government health facilities.
ABSTRACT
Polycystic ovary syndrome, which is a major cause of anovulatory infertility in women, featured by an ovarian morphology that reflects arrested follicular growth and accumulation of cystic follicles. Alteration of apoptotic process may promote development and persistence of follicular cysts, which has not been explored in details. Female animals exposed to estrogenic compounds at specific growth stages show altered pubertal maturation, ovulatory dysfunction, accumulation of follicular cysts and infertility. Here, we developed a mouse model of cystic ovary by neonatal estrogenization and investigated apoptotic changes underlying cystogenesis across various time points. We compared pro- and anti-apoptotic markers along with ovarian morphology between control and estradiol treated mice using several techniques including flow cytometry, immunohistochemistry and electron microscopy. Treated mice presented with cystic follicles with degenerated oocyte and reduced granulosa cell layer, anovulation, along with persistent estrus cycle and infertility. Increased apoptosis was demonstrated in cystic follicles with significantly increased expression of JC-1, Bid, caspase-9 and caspase-3. Thus, our findings highlight the involvement of mitochondrial pathway of apoptosis in development of polycystic ovary in response to neonatal exposure to estrogen. This model may serve to delineate the effect of environmental estrogen exposure to altered ovarian physiology which is frequently observed in PCOS women
ABSTRACT
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder of unknown etiology. Insulin resistance is very common and plays a central pathogenic role in PCOS. During last decade several studies have been conducted to understand the mechanisms contributing to the state of insulin resistance and insulin-induced hyperandrogenemia in PCOS. Insulin signaling pathways have been dissected in different insulin responsive tissues such as skeletal muscles, adipose tissues, fibroblasts as well as ovaries to elucidate the mechanism. These studies suggest a post receptor signaling defect where metabolic action of insulin is affected but not the steroidogenic and mitogenic actions. Despite advancement in these studies gaps exist in our understanding of the mechanism of insulin resistance as well as insulin-induced steroidogenesis in PCOS. The syndrome is now considered as a complex multigenic disorder. Efforts are ongoing to dissect the variants of genes from multiple logical pathways which are involved in pathophysiology of the syndrome. But still today no gene has been emerged as universally accepted susceptibility gene for PCOS. This review briefly describes the lacunae along with the current status of molecular events underlying insulin resistance and the contribution of insulin signaling pathway genes in pathogenesis of PCOS along with future researchable areas.