Gut Microbial Diversity in Women with Polycystic Ovary Syndrome Correlates with Hyperandrogenism

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Abstract

Context A majority of women with polycystic ovary syndrome (PCOS) have metabolic abnormalities that result in an increased risk of developing type 2 diabetes and heart disease. Correlative studies have shown an association between changes in the gut microbiome and metabolic disorders. Two recent studies reported a decrease in α diversity of the gut microbiome in women with PCOS compared with healthy women. Objective We investigated whether changes in the gut microbiome correlated with specific clinical parameters in women with PCOS compared with healthy women. We also investigated whether there were changes in the gut microbiome in women with polycystic ovarian morphology (PCOM) who lacked the other diagnostic criteria of PCOS. Participants Subjects were recruited at the Poznan University of Medical Sciences. Fecal microbial diversity profiles of healthy women (n = 48), women with PCOM (n = 42), and women diagnosed with PCOS using the Rotterdam criteria (n = 73) were analyzed using 16S ribosomal RNA gene sequencing. Results Lower α diversity was observed in women with PCOS compared with healthy women. Women with PCOM had a change in α diversity that was intermediate between that of the other two groups. Regression analyses showed that hyperandrogenism, total testosterone, and hirsutism were negatively correlated with α diversity. Permutational multivariate analysis of variance in UniFrac distances showed that hyperandrogenism was also correlated with β diversity. A random forest identified bacteria that discriminated between healthy women and women with PCOS. Conclusion These results suggest that hyperandrogenism may play a critical role in altering the gut microbiome in women with PCOS.

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APA

Torres, P. J., Siakowska, M., Banaszewska, B., Pawelczyk, L., Duleba, A. J., Kelley, S. T., & Thackray, V. G. (2018). Gut Microbial Diversity in Women with Polycystic Ovary Syndrome Correlates with Hyperandrogenism. Journal of Clinical Endocrinology and Metabolism, 103(4), 1502–1511. https://doi.org/10.1210/jc.2017-02153

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