scholarly journals Genetic Markers of Polycystic Ovary Syndrome: Emphasis on Insulin Resistance

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Nuzhat Shaikh ◽  
Roshan Dadachanji ◽  
Srabani Mukherjee
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Candidate Gene ◽  
Insulin Signaling ◽  
Polycystic Ovary ◽  
Women Of Childbearing Age ◽  
Childbearing Age ◽  
Ovary Syndrome ◽  
Genomic Variants ◽  
Ovulatory Dysfunction

Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting women of childbearing age causing not only reproductive but also metabolic anomalies. PCOS women present with ovulatory dysfunction, abnormal hormones, hyperandrogenemia, obesity, and hyperinsulinemia. It is a heterogeneous disorder which results from interaction of multiple genes along with environmental factors. Insulin resistance is a central key element contributing to PCOS pathogenesis and is further aggravated by obesity. Insulin regulates metabolic homeostasis and contributes to ovarian steroidogenesis. Candidate gene analyses have dissected genes related to insulin secretion and action for their association with PCOS susceptibility. Although a large number of genomic variants have been shown to be associated with PCOS, no single candidate gene has emerged as a convincing biomarker thus far. This may be attributed to large amount of heterogeneity observed in this disorder. This review presents an overview of the polymorphisms in genes related to insulin signaling and their association with PCOS and its related traits.

scholarly journals The conservative treatment in adolescents with the Polycystic ovary syndrome

2016 ◽  
Vol 11 (4) ◽  
pp. 337-341
Author(s):  
Adrian NEACȘU ◽  
◽  
Cătălina Diana STĂNICĂ ◽  
Constantin Dimitrie NANU ◽  
◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Lifestyle Modification ◽  
Polycystic Ovary ◽  
Obese Women ◽  
Metabolic Disturbances ◽  
Childbearing Age ◽  
Ovary Syndrome ◽  
Oral Antidiabetic Agents ◽  
Menstrual Cycles

Polycystic ovary syndrome (PCOS) is a common endocrine and heterogeneous dysfunction, characterized by chronic anovulation and androgen excess, affecting 6-10% of women of childbearing age. It is the most common cause of anovulatory infertility. It seems that the key element in the pathophysiology of PCOS is increased insulin resistance. The correction of infertility in teens is not a priority. They can receive treatment to normalize menstrual cycles, with the reduction of symptoms and improvement of metabolic disorders. Many overweight teens have increased insulinemia, which may play a role in the development of PCOS. Standard treatment is oral estroprogestative, used to perform regular menstrual cycles. Normalize menstrual cycles can be done with oral contraceptives or oral antidiabetic agents that improve metabolic dysfunctions. An adjuvant approach of the utmost importance for teens is lifestyle modification and diet. Teen treatment should be individualized depending on a number of peculiarities that have to be taken into account: menstruation disorders, mastopathies and ovarian dystrophies, hyperandrogenism syndrome, sexually transmitted diseases and other associated disorders. In obese women with PCOS, weight loss improves hyperandrogenism, reduces metabolic disturbances, reduces insulin resistance and insulinemia, improves fertility rate, stimulates ovulation.

scholarly journals Contemporary approaches to the management of polycystic ovary syndrome

2018 ◽  
Vol 9 (4) ◽  
pp. 123-134 ◽  
Author(s):  
Renato Pasquali
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Ovarian Function ◽  
Polycystic Ovary ◽  
Review Article ◽  
Metabolic Abnormalities ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Ovulatory Dysfunction ◽  
Ovarian Morphology

Polycystic ovary syndrome (PCOS) is a common disorder in women in their reproductive years and is characterized by androgen excess, ovulatory dysfunction, and polycystic ovarian morphology. It is also associated with several metabolic abnormalities, particularly insulin resistance and obesity, which play an important role in the pathophysiology of PCOS and, in particular, negatively influence ovarian function and fertility. This review article summarizes the available treatment for women with PCOS. Specifically, current and potentially new therapies are discussed.

scholarly journals Overexpression of Lnk in the Ovaries Is Involved in Insulin Resistance in Women With Polycystic Ovary Syndrome

Endocrinology ◽  
2016 ◽  
Vol 157 (10) ◽  
pp. 3709-3718 ◽  
Author(s):  
Meihua Hao ◽  
Feng Yuan ◽  
Chenchen Jin ◽  
Zehong Zhou ◽  
Qi Cao ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Insulin Receptor ◽  
Insulin Signaling ◽  
Fluorescent Protein ◽  
Polycystic Ovary ◽  
Adaptor Protein ◽  
Sh2 Domain ◽  
Insulin Stimulation ◽  
Ovary Syndrome

Polycystic ovary syndrome (PCOS) progression involves abnormal insulin signaling. SH2 domain-containing adaptor protein (Lnk) may be an important regulator of the insulin signaling pathway. We investigated whether Lnk was involved in insulin resistance (IR). Thirty-seven women due to receive laparoscopic surgery from June 2011 to February 2012 were included from the gynecologic department of the Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University. Samples of polycystic and normal ovary tissues were examined by immunohistochemistry. Ovarian cell lines underwent insulin stimulation and Lnk overexpression. Expressed Lnk underwent coimmunoprecipitation tests with green fluorescent protein-labeled insulin receptor and His-tagged insulin receptor substrate 1 (IRS1), and their colocalization in HEK293T cells was examined. Ovarian tissues from PCOS patients with IR exhibited higher expression of Lnk than ovaries from normal control subjects and PCOS patients without IR; mainly in follicular granulosa cells, the follicular fluid and plasma of oocytes in secondary follicles, and atretic follicles. Lnk was coimmunoprecipitated with insulin receptor and IRS1. Lnk and insulin receptor/IRS1 locations overlapped around the nucleus. IR, protein kinase B (Akt), and ERK1/2 activities were inhibited by Lnk overexpression and inhibited further after insulin stimulation, whereas IRS1 serine activity was increased. Insulin receptor (Tyr1150/1151), Akt (Thr308), and ERK1/2 (Thr202/Tyr204) phosphorylation was decreased, whereas IRS1 (Ser307) phosphorylation was increased with Lnk overexpression. In conclusion, Lnk inhibits the phosphatidylinositol 3 kinase-AKT and MAPK-ERK signaling response to insulin. Higher expression of Lnk in PCOS suggests that Lnk probably plays a role in the development of IR.

scholarly journals Local Cortisol Elevation Contributes to Endometrial Insulin Resistance in Polycystic Ovary Syndrome

2018 ◽  
Vol 103 (7) ◽  
pp. 2457-2467 ◽  
Author(s):  
Jia Qi ◽  
Wangsheng Wang ◽  
Qinling Zhu ◽  
Yaqiong He ◽  
Yao Lu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Glucose Uptake ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Polycystic Ovary ◽  
Implantation Rate ◽  
Insulin Signaling Pathway ◽  
Ovary Syndrome

Abstract Context Endometrial insulin resistance (IR) may account for the endometrial dysfunction in polycystic ovary syndrome (PCOS). The underlying mechanism remains to be elucidated. Objective To investigate whether the abundance of 11β-hydroxysteroid dehydrogenases (11β-HSDs) 1 and 2 and cortisol as well as the insulin signaling pathway are altered in PCOS endometrium and to clarify the relationship between endometrial IR and local cortisol. Design We measured cortisol and cortisone concentrations, 11β-HSD1 and 11β-HSD2, and core insulin signaling molecules in endometrial biopsies collected from non-PCOS and PCOS with or without IR patients on the seventh day after human chorionic gonadotropin injection. We also studied the effects of cortisol on glucose uptake and the insulin signaling pathway in primary cultured endometrial epithelial cells (EECs). Results The cortisol concentration was elevated, whereas 11β-HSD2 expression was diminished in endometrial biopsies obtained from PCOS with IR patients compared with those from non-PCOS and PCOS without IR patients. The implantation rate was relatively impaired and the endometrial insulin signaling pathway was defective in PCOS with IR patients. In addition, cortisol attenuated insulin-stimulated glucose uptake in EECs, which was mediated by inhibition of Akt phosphorylation and glucose transporter type 4 translocation via induction of phosphatase and tensin homolog deleted on chromosome ten (PTEN). Conclusions Decreased oxidation of cortisol and defects of insulin signaling in endometrium were observed in PCOS with IR patients. The excessive cortisol level, derived from the reduction of 11β-HSD2, might contribute to the development of endometrial IR by inhibiting the insulin signaling pathway via induction of PTEN expression in EECs.

Oxidative stress markers in women with polycystic ovary syndrome without insulin resistance

2018 ◽  
Author(s):  
Reveka Gyftaki ◽  
Sofia Gougoura ◽  
Nikolaos Kalogeris ◽  
Vasiliki Loi ◽  
George Koukoulis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Oxidative Stress Markers ◽  
Ovary Syndrome ◽  
Stress Markers
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