A distinct plasma lipidomic signature and multi-omics network in depression of polycystic ovary syndrome

Apr 2, 2026Journal of pharmaceutical and biomedical analysis

Unique blood fat patterns and related biological networks linked to depression in polycystic ovary syndrome

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Abstract

A distinct plasma lipidomic signature, characterized by the downregulation of 26 lipid species, differentiates PCOS patients with depression from those without.

Most altered lipids were triacylglycerols (TAGs) enriched with FA18:1 and FA18:2, correlating with coagulation dysfunction.
Multi-omics analysis indicated significant links between depression-associated gut bacteria, specific altered lipids, and host genes related to inflammation and metabolism.
In a mouse model, colonization by Bacteroides eggerthii increased symptoms of anhedonia and hyperlocomotion while affecting plasma IL-22 levels.
These findings suggest a complex interaction network involving gut microbiota, lipids, and host genes that may contribute to depression in PCOS.

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Patients with polycystic ovary syndrome (PCOS) are at an elevated risk of depression, yet the underlying mechanisms remain elusive. Emerging evidence implicates the gut-brain axis and systemic lipid homeostasis alterations as potential key contributors. We profiled untargeted plasma lipidomes of PCOS patients with and without comorbid depression (PCOS-DP) and integrated these data with our prior gut microbial and host transcriptomic datasets to construct multi-omics interaction networks. The causal role of the candidate gut microbial was preliminary explored in a germ-free PCOS mouse model using fecal microbiota transplantation, followed by behavioral phenotyping and ELISA-based protein quantification. We identified a distinct plasma lipidomic signature differentiating PCOS-DP from PCOS alone, characterized primarily by the downregulation of 26 lipid species. Most of these altered lipids were triacylglycerols (TAGs) enriched with FA18:1 and FA18:2, whose levels correlated with coagulation dysfunction. Multi-omics network analysis revealed significant interconnections between depression-associated gut microbiota (including Bacteroides eggerthii), specific altered lipids such as TAG (60:12/FA22:6), and host genes involved in inflammation (e.g., IL22, NLRP7), metabolism, and neural processes. Animal validation demonstrated that B. eggerthii colonization in PCOS mice specifically exacerbated anhedonia and hyperlocomotion, alongside modulating plasma IL-22 expression, suggesting its context-dependent neurobehavioral effect role. This study delineates a TAG-downregulated lipid signature with diagnostic potential and reveals a novel "gut microbiota-lipid-host gene" interaction network underpinning PCOS-DP, with B. eggerthii as a key microbial modulator of neurobehavioral phenotypes in the context of PCOS. These findings provide new pathophysiological insights and highlights potential diagnostic biomarkers for PCOS-DP.

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A distinct plasma lipidomic signature and multi-omics network in depression of polycystic ovary syndrome

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