Abstract
Polycystic ovary syndrome (PCOS) is a complex multigenic disorder and women with PCOS suffer from several comorbidities. Although, obesity is a known risk factor for PCOS, the incidence of lean women with PCOS is on the rise. A systematic and comparative study on lean and obese PCOS with respect to genes, pathways and comorbidity analysis has not been attempted so far. Analysis of differentially expressed genes (DEGs) across tissue types for lean and obese PCOS revealed that the majority of them were downregulated for lean and obese PCOS. Ovarian and endometrial tissues shared several commonly dysregulated genes, suggesting shared PCOS pathophysiology mechanisms exist across tissues. Several pathways for cellular homeostasis, such as inflammation and immune response, insulin signaling, steroidogenesis, hormonal and metabolic signaling, regulation of gonadotrophic hormone secretion, cell structure and signaling that are known to be affected in PCOS were found to be enriched in our gene expression analysis of lean and obese PCOS. The gene-disease network is denser for obese PCOS with a higher comorbidity score as compared to lean PCOS.
Highlights
Polycystic ovary syndrome (PCOS) is the most common endocrinological and metabolic disorder reported in women of reproductive age
The Gene Expression Omnibus (GEO) database was searched on 30th September 2019 to retrieve human microarray gene expression studies on PCOS using the query terms (((‘‘polycystic ovary syndrome”) AND ‘‘Homo sapiens”[Organism]) AND gse[Filter]) AND ‘‘Expression profiling by array” [Filter]. 26 datasets were identified using this query, which were further manually curated for excluding studies that involved lncRNA, drug-treated samples, cell line studies and non-body mass index (BMI) matched samples
In case of GSE98421, the BMI of the women are not provided in GEO; the study states that the tissue samples are from lean PCOS patients and this study was categorized under lean PCOS
Summary
Polycystic ovary syndrome (PCOS) is the most common endocrinological and metabolic disorder reported in women of reproductive age. The cause of the disease can be attributed to genetic and lifestyle factors [1]. The underlying pathophysiology of PCOS, based on our current understanding, can be mainly attributed to elevated LH (Luteinizing Hormone)/FSH (Follicle Stimulating Hormone) ratio and/or insulin [2]. The diagnosis of PCOS is essentially based on three features which include the presence of hyperandrogenism, menstrual irregularity and polycystic ovaries [3]. Around 30–70% of women, belonging to diverse ethnicities, are affected by PCOS and obesity [6]. 20–50% of women with PCOS are normal weight/lean and the pathophysiology may vary in these two phenotypes [7]
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