Metformin in polycystic ovary syndrome

Abstract

Polycystic ovary syndrome (PCOS) affects 6.6-6.8% of women in reproductive age. Insulin resistance and hyperinsulinemia play a critical role in the pathogenesis of PCOS and are associated with a high risk for type 2 diabetes mellitus and cardiometabolic abnormalities. Metformin has been introduced as a therapeutic option in PCOS, targeting of cardiometabolic and reproductive abnormalities on the basis of its action on the reduction of glucose levels and the attenuation of insulin resistance. The tissue-specific actions of metformin as well as the molecular mechanisms involved in the liver, the muscle, the endothelium, and the ovary are elucidated in this review. The use of metformin in pregnant women with PCOS is another of its positive features. Overall, available data supports the therapeutic usefulness of metformin on cardiometabolic risk and reproduction assistance in PCOS women.

Enhanced insulin sensitivity and acute regulation of metabolic genes and signaling pathways after a single electrical or manual acupuncture session in female insulin-resistant rats

“…Metformin is a safe and effective treatment for T2D but is associated with severe gastrointestinal side effects [9].…”

Metformin modulates human leukocyte/endothelial cell interactions and proinflammatory cytokines in polycystic ovary syndrome patients

“…In relation with this, metformin has been shown to improve biochemical and functional markers of endothelial reactivity and to reduce fibrinolysis [33]. Metformin improves vascular function via attenuation of IR/hyperinsulinemia [19], and can also decrease serum levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, by modulating androgen levels and insulin action [34]. In addition, metformin stimulates AMPK and phosphorylates endothelial nitric oxide synthase (eNOS) [19,35], while it enhances NO levels and diminishes Rho kinase in animal models of hyperlipidemia [36].…”

“…Metformin improves vascular function via attenuation of IR/hyperinsulinemia [19], and can also decrease serum levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, by modulating androgen levels and insulin action [34]. In addition, metformin stimulates AMPK and phosphorylates endothelial nitric oxide synthase (eNOS) [19,35], while it enhances NO levels and diminishes Rho kinase in animal models of hyperlipidemia [36]. However, in the present study we have no detected differences in NO levels between control and PCOS subjects either in basal conditions or after metformin treatment.…”

“…Insulin sensitizers such as metformin are widely used in the treatment of PCOS because of their capacity to improve IR [19], ovulation [20] and hyperandrogenism [21]. In addition, it has been speculated that metformin improves endothelial function in PCOS subjects [22], although conflicting results have been published regarding its effects on flow-mediated dilation in these patients [21,23].…”

Comparison of diabetes mellitus and insulin resistance screening methods for women with polycystic ovary syndrome

“…Both of these conditions have been shown to respond to treatment with insulin sensitizers in women with IR (7). The presence of IR also puts women with PCOS at increased risk for type 2 diabetes mellitus (DM).…”