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.

多囊卵巢综合征（PCOS）是一种复杂的多基因疾病，患有PCOS的女性患有多种合并症。尽管肥胖是PCOS的已知危险因素，但患有PCOS的苗条女性的发病率正在上升。迄今为止，尚未尝试对瘦型和肥胖型PCOS进行基因，途径和合并症分析方面的系统性比较研究。对瘦型和肥胖型PCOS跨组织类型的差异表达基因（DEG）的分析显示，大多数瘦型和肥胖型PCOS的基因表达下调。卵巢和子宫内膜组织共享几种常见的失调基因，这表明跨组织存在共享的PCOS病理生理机制。细胞稳态的几种途径，例如炎症和免疫反应，胰岛素信号传导，类固醇生成，激素和代谢信号传导，在我们对瘦型和肥胖型PCOS的基因表达分析中，发现已知对PCOS影响的促性腺激素分泌，细胞结构和信号传导的调控被丰富。与肥胖的PCOS相比，肥胖PCOS的基因疾病网络密度更高，合并症评分更高。