Correlation Between Fecal Metabolomics and Gut Microbiota in Obesity and Polycystic Ovary Syndrome Original paper

What was studied?

This original research article examined the fecal metabolome–microbiome signature in obese women with polycystic ovary syndrome (PCOS). The focus keyphrase fecal metabolomics in obese PCOS anchors this investigation, which integrated untargeted metabolomics with 16S rRNA sequencing to map how obesity-linked PCOS alters gut microbial composition and metabolic outputs. The study quantified 122 named differential fecal metabolites and evaluated their roles in lipid metabolism, bile acid pathways, and androgen-related signatures. It also connected these metabolites to changes in bacterial taxa and serum sex hormones, highlighting the potential microbial–metabolite–endocrine axis operating in hyperandrogenic obesity. The findings delineate a biologically meaningful cluster of fecal metabolites—particularly arachidonic acid, taurocholic acid, DHEA sulfate, eicosatrienoic acid, and docosahexaenoic acid—associated with disrupted microbial communities and heightened androgenic activity. This places gut-derived metabolic shifts as potential contributors to PCOS pathophysiology in the context of obesity.

Who was studied?

The study evaluated 33 Chinese Han women from Shanghai, including 18 obese PCOS patients and 15 obese controls without PCOS, all matched in age and BMI. Participants were 16–35 years old with BMI ≥28 kg/m² and shared similar dietary patterns standardized before sample collection. Strict exclusion criteria removed confounders such as hormonal treatments, antibiotics, probiotics, or endocrine disorders, isolating the effects of obesity and PCOS on gut microbial and metabolic signatures. This well-controlled cohort allowed clear comparisons of endocrine profiles—showing elevated testosterone, estradiol, and DHEA sulfate in PCOS—and enabled accurate mapping of how these shifts integrate with gut alterations.

Most important findings

Obese PCOS participants displayed reduced microbial richness and diversity, with notable increases in Fusobacterium, Lachnoclostridium, Tyzzerella_4, and Coprococcus_2—identified as characteristic taxa. At the phylum level, the Firmicutes/Bacteroidetes ratio decreased, and Fusobacteria increased significantly. Metabolically, PCOS samples contained elevated lipid-related metabolites, especially those tied to arachidonic acid metabolism, bile secretion, unsaturated fatty acid synthesis, and ferroptosis. Seven metabolites with high diagnostic value (VIP >3; abundance >1000) served as distinguishing features: arachidonic acid, taurocholic acid, DHEA sulfate, eicosatrienoic acid, docosahexaenoic acid, adrenic acid, and teasterone (downregulated). Correlations revealed that DHEA sulfate abundance aligned positively with serum testosterone, while teasterone showed an inverse association with serum DHEAS. Bacterial genera such as Veillonella and Lachnospira correlated strongly with elevated arachidonic-pathway metabolites, linking microbiome shifts to pro-inflammatory lipid signaling relevant to insulin resistance and ovarian dysfunction.

Key implications

The study demonstrates that obese PCOS is characterized by a tightly interwoven disturbance in gut microbiota, lipid-derived fecal metabolites, and circulating sex hormones. These findings suggest that microbiome-derived metabolic products may participate in hyperandrogenemia, inflammatory signaling, and metabolic dysregulation typical of PCOS. Characteristic metabolites—especially DHEA sulfate and arachidonic pathway lipids—and characteristic genera such as Lachnoclostridium and Fusobacterium offer potential signatures for microbiome-based diagnostics or therapeutic targeting. The work strengthens the rationale for integrating microbiome modulation into PCOS management strategies, particularly in obese phenotypes marked by hormonal–microbial–metabolic crosstalk.

Citation

Zhou L, Ni Z, Yu J, Cheng W, Cai Z, Yu C. Correlation between fecal metabolomics and gut microbiota in obesity and polycystic ovary syndrome. Front Endocrinol (Lausanne). 2020;11:628. doi:10.3389/fendo.2020.00628. fendo-11-00628