a year ago
Impact of Visceral Obesity on Structural and Functional Alterations of Gut Microbiota in Polycystic Ovary Syndrome (PCOS): A Pilot Study Using Metagenomic Analysis
Xuefeng Bai,1,* Jiangxin Ma,1,* Xiaohong Wu,1 Lingling Qiu,2 Rongfu Huang,3 Haibin Zhang,1 Huibin Huang,1 Xiaoyu Chen1
1Department of Endocrinology, Second Affiliated Hospital of Fujian Medical University, Quanzhou City, Fujian Province, People's Republic of China; 2Department of Reproductive Medicine, Second Affiliated Hospital of Fujian Medical University, Quanzhou City, Fujian Province, People's Republic of China; 3Department of Clinical Laboratory, Second Affiliated Hospital of Fujian Medical University, Quanzhou City, Fujian Province, People's Republic of China
*These authors contributed equally to this work
Correspondence: Huibin Huang; Xiaoyu Chen, Department of Endocrinology, the Second Affiliated Hospital of Fujian Medical University, No. 950 Donghai Street, Fengze District, Quanzhou City, Fujian Province, 362000, People's Republic of China, Tel +86-13313872001 ; +86-13600739755, Email ;
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<-0.4, 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.
Keywords: polycystic ovary syndrome, visceral obesity, gut microbiota, visceral fat area, metagenomic analysis Polycystic ovary syndrome (PCOS) is a highly prevalent disease in reproductive-aged women, characterized by menstrual disorder, abnormally high androgen, polycystic ovary morphology, and infertility.1 Although genetic, gestational environmental and lifestyle factors are thought to be involved in the development of PCOS, how do these factors pathologically trigger biochemical and metabolic disorders remains widely unknown. Limited therapeutic options have focused mainly on symptoms, resulting in unsatisfactory treatment outcomes and long-term metabolic complications. Therefore, there is an urgent need to develop new therapeutic strategies. Recent studies have reported alterations of gut microbiota in PCOS patients2–5 and provided convincing evidence for a causal correlation between dysbiosis of gut microbiota and onset of ovarian and metabolic dysfunction.2,4 Dysbiosis of gut microbiota can increase secretion of ovarian androgen, which then interfere normal follicular development by triggering a chronic inflammatory response and insulin resistance.6 Further evidence has suggested that gut microbiota and their metabolites can cause imbalances in energy intake, activate inflammatory pathways, stimulate secretion of brain gut peptides, and proliferate pancreatic β-cells, leading to abnormal or excessive fat accumulation, insulin resistance, and compensatory hyperinsulinemia.2,7 Fecal microbiota transplantation (FMT) from the healthy, addition of probiotics, alteration of bile acid metabolism, and/or increasing IL-22 level have been demonstrated to be valuable in treatment for PCOS
1Department of Endocrinology, Second Affiliated Hospital of Fujian Medical University, Quanzhou City, Fujian Province, People's Republic of China; 2Department of Reproductive Medicine, Second Affiliated Hospital of Fujian Medical University, Quanzhou City, Fujian Province, People's Republic of China; 3Department of Clinical Laboratory, Second Affiliated Hospital of Fujian Medical University, Quanzhou City, Fujian Province, People's Republic of China
*These authors contributed equally to this work
Correspondence: Huibin Huang; Xiaoyu Chen, Department of Endocrinology, the Second Affiliated Hospital of Fujian Medical University, No. 950 Donghai Street, Fengze District, Quanzhou City, Fujian Province, 362000, People's Republic of China, Tel +86-13313872001 ; +86-13600739755, Email ;
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<-0.4, 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.
Keywords: polycystic ovary syndrome, visceral obesity, gut microbiota, visceral fat area, metagenomic analysis Polycystic ovary syndrome (PCOS) is a highly prevalent disease in reproductive-aged women, characterized by menstrual disorder, abnormally high androgen, polycystic ovary morphology, and infertility.1 Although genetic, gestational environmental and lifestyle factors are thought to be involved in the development of PCOS, how do these factors pathologically trigger biochemical and metabolic disorders remains widely unknown. Limited therapeutic options have focused mainly on symptoms, resulting in unsatisfactory treatment outcomes and long-term metabolic complications. Therefore, there is an urgent need to develop new therapeutic strategies. Recent studies have reported alterations of gut microbiota in PCOS patients2–5 and provided convincing evidence for a causal correlation between dysbiosis of gut microbiota and onset of ovarian and metabolic dysfunction.2,4 Dysbiosis of gut microbiota can increase secretion of ovarian androgen, which then interfere normal follicular development by triggering a chronic inflammatory response and insulin resistance.6 Further evidence has suggested that gut microbiota and their metabolites can cause imbalances in energy intake, activate inflammatory pathways, stimulate secretion of brain gut peptides, and proliferate pancreatic β-cells, leading to abnormal or excessive fat accumulation, insulin resistance, and compensatory hyperinsulinemia.2,7 Fecal microbiota transplantation (FMT) from the healthy, addition of probiotics, alteration of bile acid metabolism, and/or increasing IL-22 level have been demonstrated to be valuable in treatment for PCOS
-Abstract Truncated-
Publisher URL: https://www.dovepress.com/impact-of-visceral-obesity-on-structural-and-functional-alterations-of-peer-reviewed-fulltext-article-DMSO
DOI: 10.2147/DMSO.S388067
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