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Home > Archives > Volume 20, No 8 (2022) > Article

DOI: 10.14704/nq.2022.20.8.NQ44583

Insulin Resistance (IR) in Women with Polycystic Ovary Syndrome (PCOS)

Ali El-shabrawy Ali, Ahmad Nader Mohammed Mustafa, Ahmed Mohammed Baraka, Mostafa Abdo Ahmed

Abstract

Background: There are reports which say 65–95% of all the women have PCOS also have insulin resistance which might be due to perturbed receptor tyrosine kinase, or other protein of insulin signaling cascade, modified adipokine signaling, and its secretion when compared to normal women. In addition, the prevalence of type II diabetes is increased in women with PCOS compared with women without PCOS (15% vs. 2.3%). It is now clearly established that insulin resistance is present in obese and non-obese women with PCOS; however, the exact mechanism of insulin resistance in PCOS remain elusive. Recent studies on mechanisms of insulin resistance in PCOS have focused on polymorphisms in genes regulating carbohydrate homeostasis. However, none of these genes have been consistently shown to be related with PCOS. One central paradox regarding insulin resistance in PCOS is the high responsiveness to insulin by the ovary, as opposed to the resistance of the whole body, and this model has been used to explain ovarian hyperandrogenemia as it though to arise from a direct stimulatory effect of insulin on ovarian stromal cells. However, a study from China on women with PCOS appears to contradict this hypothesis suggesting that ovarian cells are also insulin resistant. Insulin resistance is characterized by a post-receptor defect in the action of insulin, the cause of which is still being elucidated. The first step in the action of insulin involves binding to the cell-surface receptor. Following insulin binding, the receptor undergoes autophosphorylation on specific tyrosine residues (accomplished by activation of insulin receptor tyrosine kinase IRTK). The activated receptor then activates insulin receptor substrates (such as IRS1, 2, and 3) that in turn bind to signaling molecules (such as phosphatidylinositol-3 kinase) and activate downstream signaling leading to insulin-mediated glucose transport

Keywords

Insulin Resistance, Polycystic Ovary Syndrome

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