Abstract
Polycystic ovary syndrome (PCOS) is one of the most common endocrine diseases among women of reproductive age and is associated with many metabolic manifestations, such as obesity, insulin resistance (IR) and hyperandrogenism. The underlying pathogenesis of these metabolic symptoms has not yet been fully elucidated. With the application of metabolomics techniques, a variety of metabolite changes have been observed in the serum and follicular fluid (FF) of PCOS patients and animal models. Changes in metabolites result from the daily diet and occur during uncommon physiological routines. However, some of these metabolite changes may provide evidence to explain possible mechanisms and new approaches for prevention and therapy. This article reviews the pathogenesis of PCOS metabolic symptoms and the relationship between metabolites and the pathophysiology of PCOS. Furthermore, the potential clinical application of some specific metabolites will be discussed.
Highlights
Polycystic ovary syndrome (PCOS) is one of the most complicated and heterogeneous endocrine disorders, with a prevalence ranging from approximately 6% to 20% in women of reproductive age [1,2,3]
We further demonstrated that glycodeoxycholic acid (GDCA) and tauroursodeoxycholic acid (TUDCA) were decreased due to the deconjugation of bile salt hydrolase (BSH) in PCOS patients and that supplementation with these bile acids can improve the PCOS phenotype by activating transmembrane G coupled receptor 5 (TGR5) and further enhancing IL-22 secretion by intestinal Group 3 innate lymphoid cells (ILC3s) [58]
In a prospective study of 27 obese patients with PCOS, Eyupoglu et al found for the first time that trimethylamine N-oxide (TMAO) and its precursors are elevated in women with PCOS compared with in healthy women, which seems to indicate that TMAO is associated with hyperandrogenism in PCOS [118]
Summary
Polycystic ovary syndrome (PCOS) is one of the most complicated and heterogeneous endocrine disorders, with a prevalence ranging from approximately 6% (applying the older diagnostic criteria: National Institutes of Health Consensus 1990) to 20% (according to the current most commonly used criteria: the Rotterdam 2003) in women of reproductive age [1,2,3]. There are three criteria included in actual diagnostic criteria, including the Rotterdam 2003, the Androgen Excess and PCOS Society 2006 and National Institutes of Health Consensus 2012. A woman with PCOS must meet at least two of the three characteristics, and other causes of hyperandrogenism, such as nonclassical congenital adrenal hyperplasia and hyperprolactinemia, must be ruled out [5] According to these diagnostic criteria, PCOS is divided into four phenotypes according to severity [6,7] (Table 1). PCOS shows heterogeneity in regard to metabolic disorders [1] This background indicates that the daily lifestyle and diet as well as metabolites generated may have a substantial influence on the pathogenesis of PCOS.
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