Polycystic ovary syndrome (PCOS) and endocrine disrupting chemicals (EDCs)

Palioura, Eleni; Diamanti-Kandarakis, Evanthia

doi:10.1007/s11154-016-9326-7

Cited by 120 publications

(71 citation statements)

References 73 publications

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“…However, it is believed that the most likely vulnerable period of exposure is in utero and the first few years of life (26). The reasoning proposes that animal studies of exogenous androgen exposure and human evidence of in utero growth restriction with subsequent catch-up growth, leading to the subsequent development of features of PCOS and the metabolic syndrome, suggest that a period of vulnerability exists at this time to individuals who may have a genetic predisposition to PCOS (26,246). Indeed, with the use of both high-and low-dose exposures to BPA in early postnatal life, a rodent model of PCOS has been developed (103).…”

Section: Influences On Follicular Development and Ovulationmentioning

confidence: 99%

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Hart

2016

Physiological Reviews

168

119

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Across the Western World there is an increasing trend to postpone childbearing. Consequently, the negative influence of age on oocyte quality may lead to a difficulty in conceiving for many couples. Furthermore, lifestyle factors may exacerbate a couple's difficulty in conceiving due mainly to the metabolic influence of obesity; however, the negative impacts of low peripheral body fat, excessive exercise, the increasing prevalence of sexually transmitted diseases, and smoking all have significant negative effects on fertility. Other factors that impede conception are the perceived increasing prevalence of the polycystic ovary syndrome, which is further exacerbated by obesity, and the presence of uterine fibroids and endometriosis (a progressive pelvic inflammatory disorder) which are more prevalent in older women. A tendency for an earlier sexual debut and to have more sexual partners has led to an increase in sexually transmitted diseases. In addition, there are several genetic influences that may limit the number of oocytes within the ovary; consequently, by postponing attempts at childbearing, a limitation of oocyte number may become evident, whereas in previous generations with earlier conception this potentially reduced reproductive life span did not manifest in infertility. Environmental influences on reproduction are under increasing scrutiny. Although firm evidence is lacking however, dioxin exposure may be linked to endometriosis, phthalate exposure may influence ovarian reserve, and bisphenol A may interfere with oocyte development and maturation. However, chemotherapy or radiotherapy is recognized to lead to ovarian damage and predispose the woman to ovarian failure.

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Section: Influences On Follicular Development and Ovulationmentioning

confidence: 99%

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Hart

2016

Physiological Reviews

168

119

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“…Women with PCOS or T2DM are reported to have ovarian dysfunction, low implantation rates, slow development, and high miscarriage rates [1,[17][18][19]. However, the underlying mechanism of this phenomenon is still unknown.…”

Section: Animal Model and Tissue Collectionmentioning

confidence: 99%

High insulin impaired ovarian function in early pregnant mice and the role of autophagy in this process

et al. 2017

Endocr J

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METABOLIC DISORDERS, such as PCOS (polycystic ovary syndrome) and T2DM (type 2 diabetes mellitus), are reported to be associated with high miscarriage rates, decreased pregnancy rates, and low live birth rates [1]. PCOS and T2DM are characterized by hyperinsulinemia [2]. PCOS is an endocrine and metabolic disorder with a prevalence ranging from 5 to 13% in women of reproductive age. Moreover, PCOS is often accompanied by menstrual dysfunction, anovulaHigh insulin impaired ovarian function in early pregnant mice and the role of autophagy in this process Abstract. Metabolic disorders, such as PCOS (polycystic ovarian syndrome) and T2DM (type 2 diabetes mellitus), are associated with menstrual dysfunction, anovulation, infertility, and early pregnancy loss. Ovarian dysfunction is not only related to low pregnancy rates but also to the increased risk of miscarriage. Women with PCOS or T2DM, characterized by hyperinsulinemia, commonly experience ovarian dysfunction. In this study, we first explored whether high insulin levels directly affected ovarian functioning during embryo implantation. Mice in the insulin-treated group were given a subcutaneous injection of human recombinant insulin. After insulin treatment, serum levels of E2 (estrogen), PROG (progesterone), LH (luteinizing hormone), and FSH (follicle-stimulating hormone) were obviously lower, and there was a significant decrement of ovarian GDF9 (growth differentiation factor 9) mRNA. H&E (hematoxylin and eosin) staining showed a greater number of immature follicles and less luteinization in the insulin group. Further autophagy was studied in this process. A significant increase of P62 (SQSTM1/Sequestosome1) and a decrease of Cathepsin B, BECN1 (Beclin 1), and ULK1 (Unc-51-like kinase 1) mRNA in ovary was found in the insulin group. Western blot analysis showed that the expressions of LC3 (microtubule-associated protein 1 light chain 3), BECN1, and Cathepsin B proteins in ovaries from insulin group were obviously reduced, while P62 proteins were significantly increased. All these results illustrated that insulin could directly impair ovarian function during embryo implantation and the imbalance of ovarian autophagy due to insulin. Autophagy could enhance the impaired ovarian function results from insulin.

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“…Clinical data demonstrate increased levels of BPA in patients with PCOS [25], and the levels can reach those in males [26]. PCOS induced by BPA exposure is also associated with hyperandrogenism and hyperinsulinism.…”

Section: Introductionmentioning

confidence: 98%

Bisphenol-A Dose-dependently Regulates The Development of Ovary and Uterus through Differential Expression of METTL3

Zhang

Zhu

Zhang

et al. 2020

Preprint

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Background: Environmental endocrine disruptors, which have a profound impact on the reproductive system, can cause endocrine and reproductive disorders, such as polycystic ovary syndrome (PCOS). Bisphenol-A (BPA) is a common endocrine disruptor which can affect the function of the reproductive system under low-dose conditions. However, the mechanism by which this molecule disrupts normal reproduction is still unclear. In this study, we investigated the effects of BPA on the RNA methyltransferase METTL3 in adolescent female rats which may be a possible mode of action of BPA. Methods: 4-week-old Sprague-Dawley (SD) rats were intragastrically treated for 10 weeks, which were divided into blank group (n = 8), control group (soybean oil, n = 8), three BPA-treatment groups (0.5 mg/kg BPA + soybean oil, 5 mg/kg BPA + soybean oil, 50 mg/kg BPA + soybean oil, n = 8). Results: The results showed that low-dose BPA (0.5 mg/kg) increased the coefficient of uteri and ovaries, and promoted the growth of uteri in rats without causing hyperandrogenism and ovarian polycystic changes. Oral BPA disturbed the expression of CYP17A1, CYP11A1 and METTL3 in ovaries and effected the level of serum testosterone. Conclusions: Our results suggested that oral BPA might interfere uterine and ovarian morphology and the level of hormone with RNA methylation by disturbing the expression level of METTL3. RNA methylation will be a new way to explain the interference mechanism of BPA.

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Polycystic ovary syndrome (PCOS) and endocrine disrupting chemicals (EDCs)

Cited by 120 publications

References 73 publications

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

High insulin impaired ovarian function in early pregnant mice and the role of autophagy in this process

Bisphenol-A Dose-dependently Regulates The Development of Ovary and Uterus through Differential Expression of METTL3

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