Impact of Visceral Obesity on Structural and Functional Alterations of Gut Microbiota in Polycystic Ovary Syndrome (PCOS): A Pilot Study Using Metagenomic Analysis.

aimed to identify structural and functional alterations of gut microbiota associated with visceral obesity in adult women with polycystic ovary syndrome (PCOS). Methods: Twenty-seven adults with PCOS underwent stool and fasting blood collection, oral glucose tolerance testing, and visceral fat area (VFA) measurement via dual-bioimpedance technique. Metagenomic analysis was used to analyze gut microbiota. Results: PCOS patients were divided into three groups: visceral obesity group (PCOS-VO, n=9, age 28.33± 5.68 years, BMI 37.06± 4.27 kg/m², VFA 128.67± 22.45 cm²), non-visceral obesity group (PCOS-NVO, n=10, age 25.40± 4.53, BMI 30.74± 3.95, VFA 52.00± 24.04), normal BMI group (PCOS-NB, n=8, age 27.88± 2.53, BMI 21.56± 2.20, VFA 27.00± 21.18), with no statistical difference in age (P> 0.05) and significantly statistical differences in BMI and VFA (P< 0.05). The groups showed a significant difference in microbial β-diversity between PCOS-VO and PCOS-NVO (P=0.002) and no difference between PCOS-NVO and PCOS-NB (P=0.177). Bacteroidetes was the phylum with the highest relative abundance among all patients, followed by Firmicutes. Those with visceral obesity had a higher abundance of Prevotella, Megamonas, and Dialister genera, positively correlated with metabolic markers (r> 0.4, P< 0.05), and lower abundance of Phascolarctobacterium and Neisseria genera, negatively correlated with metabolic markers (r<-0.4, P< 0.05). Functional annotation analysis showed significant differences in relative abundance of ribosome pathway, fatty acid biosynthesis pathway, and sphingolipid signaling pathway between groups, affecting lipid homeostasis and visceral fat accumulation. Conclusion: Alteration in β-diversity of gut microbiota exists in PCOS with visceral obesity versus those without visceral obesity and relates to functional differences in ribosomes, fatty acid biosynthesis, and sphingolipid signaling pathways. [ABSTRACT FROM AUTHOR]