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

Abstract

Objective: We 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 <0.05). 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.