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      Association between The Number of Retrieved Mature Oocytes and Insulin Resistance or Sensitivity in Infertile Women Polycystic Ovary Syndrome

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          Abstract

          Background

          The objective of this study was to describe the association between luteinizing hormone (LH)/ follicle-stimulating hormone (FSH) ratio and demographic variables and maturation stage of oocytes in insulin- resistant and insulin-sensitive patients with polycystic ovary syndrome (PCOS) in comparison with control group.

          Materials and Methods

          In this case-control study, 60 patients with in vitro fertilization (IVF)/intracytoplas- mic sperm injection (ICSI) indication were subdivided into 3 groups as follow: 20 subjects were assigned to control (fertile women with male infertility history) group, 20 subjects with PCOS were insulin resistant (IR) and 20 subjects with PCOS were insulin sensitive (IS). After puncture, retrieved oocytes were classified into metaphase II (MII) as mature and in metaphase I (MI) or germinal vesicle stage (GV) as immature. Regres- sion analyses were used to explore the association between MII oocyte number and demographic and clinical variables.

          Results

          LH/FSH ratio was significantly higher in PCOS-IR women compared to controls but not significantly dif- ferent from that of PCOS-IS group. PCOS-IR women had lower MII oocyte number compared with that of controls. According to multiple regression analysis, the number of previous assisted reproductive technology (ART) cycles was negatively associated with the number of MII oocytes.

          Conclusion

          Insulin resistance can be associated with reductions in MII oocyte number in patients with PCOS.

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          Most cited references32

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          Prevalence, phenotype and cardiometabolic risk of polycystic ovary syndrome under different diagnostic criteria.

          What is the prevalence, phenotype and metabolic features of polycystic ovary syndrome (PCOS) in the same population according to three different diagnostic criteria? The prevalence of PCOS under National Institutes of Health (NIH), Rotterdam and Androgen Excess and PCOS (AE-PCOS) Society criteria was 6.1, 19.9 and 15.3%, respectively. PCOS carried a 2-fold increased risk of metabolic syndrome regardless of the diagnostic criteria used. The prevalence rates of PCOS differ depending on the diagnostic criteria used to define the syndrome. The current paper gives the prevalence rates of the component and composite phenotypes of PCOS in the same population and reports similar rates of metabolic syndrome in women with PCOS under contrasting diagnostic criteria. In this cross-sectional study, 392 women between the ages of 18 and 45 years were analyzed. When the prevalence of PCOS according to NIH was set to 8% with a precision of 2.2% and confidence interval of 95%, the sample size required for a prevalence survey was found to be 400 subjects. The study was carried out in the General Directorate of Mineral Research and Exploration, a government-based institute, in which the largest number of female staff (n = 527) are employed within a single institute in Ankara, Turkey. The study was performed between 7 December 2009 and 30 April 2010. All female subjects between the ages of 18 and 45 years were invited to participate. Women older than 45 or younger than 18 years, post-menopausal women, women with a history of hysterectomy or bilateral oopherectomy and pregnant women were excluded. Totally, 392 of the employees were recruited for the final analyses. The prevalence of PCOS under NIH, Rotterdam and AE-PCOS Society criteria were 6.1, 19.9 and 15.3%, respectively. While the prevalence of metabolic syndrome was 6.1% in the whole study group, within the patients diagnosed as PCOS according to NIH, Rotterdam and AE-PCOS Society criteria, it was 12.5, 10.3 and 10.0%, respectively. Even though we have included women working at a single institution with a high response rate for the participation, we cannot exclude potential selection bias due to undetermined differences between our sample and background community. We might have underestimated actual prevalence of metabolic syndrome in PCOS due to lack of oral glucose tolerance test 2 h glucose data. Current results can be generalized to Caucasian populations and may present variations in other populations according to race and ethnicity. This work was, in part, sponsored by Merck Serono. Not applicable.
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            Multiple signaling pathways regulating steroidogenesis and steroidogenic acute regulatory protein expression: more complicated than we thought.

            Steroid hormone biosynthesis in steroidogenic cells is regulated through trophic hormone activation of protein kinase A (PKA) signaling pathways. However, many examples of the regulation of steroid synthesis via pathways other than the PKA pathway have been documented. In some cases these pathways act independently of PKA activation whereas in other cases, they act synergistically with it. The current understanding of additional signaling pathways and factors, such as the protein kinase C pathway, arachidonic acid metabolites, growth factors, chloride ion, the calcium messenger system, and others capable of regulating/modulating steroid hormone biosynthesis, and in many cases steroidogenic acute regulatory protein expression, are discussed in this review.
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              Insulin signalling and glucose transport in the ovary and ovarian function during the ovarian cycle

              Data derived principally from peripheral tissues (fat, muscle and liver) show that insulin signals via diverse interconnecting intracellular pathways and that some of the major intersecting points (known as critical nodes) are the IRSs (insulin receptor substrates), PI3K (phosphoinositide kinase)/Akt and MAPK (mitogen-activated protein kinase). Most of these insulin pathways are probably also active in the ovary and their ability to interact with each other and also with follicle-stimulating hormone (FSH) and luteinizing hormone (LH) signalling pathways enables insulin to exert direct modulating influences on ovarian function. The present paper reviews the intracellular actions of insulin and the uptake of glucose by ovarian tissues (granulosa, theca and oocyte) during the oestrous/menstrual cycle of some rodent, primate and ruminant species. Insulin signals through diverse pathways and these are discussed with specific reference to follicular cell types (granulosa, theca and oocyte). The signalling pathways for FSH in granulosa cells and LH in granulosa and theca cells are summarized. The roles of glucose and of insulin-mediated uptake of glucose in folliculogenesis are discussed. It is suggested that glucose in addition to its well-established role of providing energy for cellular function may also have insulin-mediated signalling functions in ovarian cells, involving AMPK (AMP-dependent protein kinase) and/or hexosamine. Potential interactions of insulin signalling with FSH or LH signalling at critical nodes are identified and the available evidence for such interactions in ovarian cells is discussed. Finally the action of the insulin-sensitizing drugs metformin and the thiazolidinedione rosiglitazone on follicular cells is reviewed.
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                Author and article information

                Journal
                Int J Fertil Steril
                Int J Fertil Steril
                Royan Institute
                International Journal of Fertility & Sterility
                Royan Institute
                2008-076X
                2008-0778
                Jan-Mar 2019
                02 October 2018
                : 12
                : 4
                : 310-315
                Affiliations
                [1 ]Department of Animal Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran
                [2 ]Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
                [3 ]Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
                [4 ]Department of Endocrinology and Female Infertility, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
                [5 ]Department of Obstetrics and Gynecology, Arash Women’s Hospital, Tehran University of Medical Sciences, Tehran, Iran
                [6 ]Department of Epidemiology and Reproductive Health, Reproductive Epidemiology Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
                Author notes
                [*Corresponding Addresses: ]P.O.Box: 15719-14911Department of Animal BiologyFaculty of Biological SciencesKharazmi University TehranIranP.O.Box: 16635-148Department of EmbryologyReproductive Biomedicine Research CenterRoyan Institute for Reproductive Biomedicine ACECRTehranIran Emails: fateme.hassani@ 123456gmail.com , eftekhari@ 123456royaninstitute.org
                Article
                Int-J-Fertil-Steril-12-310
                10.22074/ijfs.2019.5422
                6186286
                30291692
                e47dd32d-bf40-4fe7-8c70-19c8d5e3c474
                Any use, distribution, reproduction or abstract of this publication in any medium, with the exception of commercial purposes, is permitted provided the original work is properly cited

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 September 2017
                : 5 May 2018
                Categories
                Original Article
                Embryology
                Gynecology and Female Infertility
                Custom metadata
                Hassani F, Oryan S, Eftekhari-Yazdi P, Bazrgar M, Moini A, Nasiri N, Ghaheri A. Association between the number of retrieved mature oocytes and insulin resistance or sensitivity in infertile women polycystic ovary syndrome. Int J Fertil Steril. 2019; 12(4): 310-315. doi: 10.22074/ijfs.2019.5422.

                assisted reproductive technology,insulin resistance,oocyte,polycystic ovary syndrome

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