MicroRNAs related to androgen metabolism and polycystic ovary syndrome

Anja Elaine Sørensen, Pernille Bækgaard Udesen, Marie Louise Wissing, Anne Lis Mikkelsen Englund, Louise Torp Dalgaard

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review


Polycystic ovary syndrome (PCOS) is a frequent endocrine disorder in women. PCOS is associated with altered features of androgen metabolism, increased insulin resistance and impaired fertility. Furthermore, PCOS, being a syndrome diagnosis, is heterogeneous and characterized by polycystic ovaries, chronic anovulation and evidence of hyperandrogenism, as well as being associated with chronic lowgrade inflammation and an increased life time risk of type 2 diabetes. A number of androgen species contribute to the symptoms of increased androgen exposure seen in many, though not all, cases of PCOS:
Testosterone, androstenedione, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS), where the quantitatively highest amount of androgen is found as DHEAS. The sulfation of DHEA to DHEAS depends on a number of enzymes, and altered sulfate metabolism may be associated with and contribute to the pathogenesis of PCOS.
MicroRNAs (miRNAs) are small, non-coding RNAs that are able to regulate gene expression at the posttranscriptional level. Altered miRNA levels have been associated with diabetes, insulin resistance, inflammation and various cancers. Studies have shown that circulating miRNAs are present in whole blood, serum, plasma and the follicular fluid of PCOS patients and that these might serve as potential biomarkers and a new approach for the diagnosis of PCOS. In this review, recent work on miRNAs with respect to PCOS will be summarized. Our understanding of miRNAs, particularly in relation to PCOS, is currently at a very early stage, and additional studies will yield important insight into the molecular
mechanisms behind this complex and heterogenic syndrome.
TidsskriftChemico-Biological Interactions
Sider (fra-til)8-16
Antal sider9
StatusUdgivet - 2016

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