Exposure to a Healthy Gut Microbiome Protects Against Reproductive and Metabolic Dysregulation in a PCOS Mouse Model
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ABSTRACT:
PROVIDER: PRJEB29583 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2882332_1.fastq.gz | Fastqsanger.gz | |||
| ERR2882332_2.fastq.gz | Fastqsanger.gz |
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Project description:Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting ∼10% to 15% of reproductive-aged women worldwide. Diagnosis requires two of the following: hyperandrogenism, oligo-ovulation or anovulation, and polycystic ovaries. In addition to reproductive dysfunction, many women with PCOS display metabolic abnormalities associated with hyperandrogenism. Recent studies have reported that the gut microbiome is altered in women with PCOS and rodent models of the disorder. However, it is unknown whether the gut microbiome plays a causal role in the development and pathology of PCOS. Given its potential role, we hypothesized that exposure to a healthy gut microbiome would protect against development of PCOS. A cohousing study was performed using a letrozole-induced PCOS mouse model that recapitulates many reproductive and metabolic characteristics of PCOS. Because mice are coprophagic, cohousing results in repeated, noninvasive inoculation of gut microbes in cohoused mice via the fecal-oral route. In contrast to letrozole-treated mice housed together, letrozole mice cohoused with placebo mice showed significant improvement in both reproductive and metabolic PCOS phenotypes. Using 16S rRNA gene sequencing, we also observed that the overall composition of the gut microbiome and the relative abundance of Coprobacillus and Lactobacillus differed in letrozole-treated mice cohoused with placebo mice compared with letrozole mice housed together. These results suggest that dysbiosis of the gut microbiome may play a causal role in PCOS and that modulation of the gut microbiome may be a potential treatment option for PCOS.
| S-EPMC6482036 | biostudies-literature
Project description:Polycystic ovary syndrome (PCOS) is typically characterized by oligo or anovulation, hyperandrogenism and polycystic ovarian morphology, affecting 5-20% of women of reproductive age [1]. It has drawn significant attention as a major cause of anovulatory infertility and the syndrome of metabolic, reproductive and obstetrical disorders [2 ,+]. Due to heterogeneous clinical features and unclear pathogenesis of PCOS, the diagnosis and treatment strategies remain a matter of debate. To better understand the complex follicular development environment in PCOS, we conducted a TMT-based quantitative proteomic study to compare the composition of proteins, pathways and molecular functions of FF from lean and overweight/obese women with PCOS and that of healthy controls.
2019-10-31 | PXD013937 | Pride
Project description:Transcriptomic and genome-wide DNA methylation was performed on T helper cells using RNA-sequencing and Reduced Representation Bisulfite Sequencing, respectively. Specific genome-wide DNA methylation analysis of T helper cells from women with PCOS identified 5,581 differentially methylated CpG sites. Interestingly, functional gene ontology enrichment analysis showed that genes located at the proximity of differentially methylated CpG sites belong to pathways related to reproductive function and immune cell function. However, these genes were not altered at the transcriptomic level. Our results show that PCOS is associated with global and gene-specific DNA methylation remodelling in a cell-type specific manner.
2019-08-22 | GSE130581 | GEO
Project description:Transcriptomic and genome-wide DNA methylation was performed on T helper cells using RNA-sequencing and Reduced Representation Bisulfite Sequencing, respectively. Specific genome-wide DNA methylation analysis of T helper cells from women with PCOS identified 5,581 differentially methylated CpG sites. Interestingly, functional gene ontology enrichment analysis showed that genes located at the proximity of differentially methylated CpG sites belong to pathways related to reproductive function and immune cell function. However, these genes were not altered at the transcriptomic level. Our results show that PCOS is associated with global and gene-specific DNA methylation remodelling in a cell-type specific manner.
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Project description:This experiment was designed to study if there are differences in gene expression in the adipose tissue of women affected by polycystic ovary syndrome (PCOS) compared to non-hyperandrogenic women. PCOS is the most common endocrinopathy in women of reproductive age, and is characterized by hyperandrogenism and chronic anovulation. This disease is frequently associated with obesity, insulin resistance, and defects in insulin secretion, predisposing these women to type 2 diabetes, atherosclerosis, and cardiovascular disease. We have applied high-density oligonucleotide arrays to omental adipose tissue samples obtained from eight morbidly obese PCOS patients and seven morbidly obese non-PCOS women at the time of bariatric surgery. Keywords: Disease state analysis
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Project description:Hepatocyte polyploidization during ageing protects against transcriptional dysregulation and chronic liver disease
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Project description:To reveal microRNAs expression differences in cumulus cells between polycystic ovary syndrome (PCOS) and non-PCOS women. miRNAs expression profile of the cumulus cell samples with PCOS and non-PCOS were determined by Affymetrix miRNA 2.0. Six pooled RNAs from CC samples (three PCOS and three non-PCOS pooled RNAs) were separately analyzed on 6 GeneChip miRNA 2.0 Array (miRBase V15)
2015-04-28 | E-GEOD-68285 | biostudies-arrayexpress
Project description:Insulin resistance is a common metabolic abnormality in women with PCOS and leads to an elevated risk of type 2 diabetes. Studies have shown that thiazolidinediones (TZD) improve metabolic disturbances in PCOS patients. We hypothesized that the effect of TZD in PCOS is in part mediated by changes in the transcriptional profile of muscle favoring insulin sensitivity. Using Affymetrix microarrays, we examined the effect of pioglitazone (30 mg/day for 16 weeks) on gene expression in skeletal muscle of 10 obese women with PCOS metabolically characterized by a euglycemic-hyperinsulinemic clamp. Moreover, we explored gene expression changes between these PCOS patients before treatment and 13 healthy control women. Treatment with pioglitazone improved insulin-stimulated total, oxidative and non-oxidative glucose metabolism, and reduced fasting serum insulin (all p < 0.05). Global pathway analysis using Gene Map Annotator and Pathway Profiler (GenMAPP 2.1) and Gene Set Enrichment Analysis (GSEA 2.0.1) revealed a significant upregulation of genes involved in mitochondrial oxidative phosphorylation (OXPHOS), ribosomal proteins, mRNA processing reactome, translation factors, and proteasome complexes in PCOS patients after pioglitazone therapy. Quantitative real-time PCR suggested that upregulation of OXPHOS genes was mediated by an increase in PGC-1M-NM-1 expression (p < 0.05). Expression of genes involved in ribosomal proteins and OXPHOS was down-regulated in PCOS patients before treatment compared to matched healthy women using GenMAPP 2.1 and GSEA 2.1. These data indicate that pioglitazone therapy restores insulin sensitivity in part by a coordinated upregulation of genes involved in mitochondrial oxidative metabolism and protein biosynthesis in skeletal muscle of PCOS. These transcriptional effects of pioglitazone therapy may contribute to prevent the onset of type 2 diabetes in these women. Experiment Overall Design: Ten obese women of reproductive age with PCOS participated in the study to test the effect of pioglitazone therapy (data set 1). To test if pioglitazone ameliorate existing defects in PCOS patients, the expression profile of the 10 PCOS patients before treatment were compared to the same cohort of 13 control subjects (data set 2).
2008-11-14 | E-GEOD-8157 | biostudies-arrayexpress
Project description:Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder affecting women of reproductive age. The main features of PCOS are hyperandrogenism and irregular menstrual cycles together with metabolic dysfunctions including abdominal obesity, dyslipidemia and an increased risk of developing type 2 diabetes. Despite the high prevalence of >15%, the pathophysiology of the syndrome is unclear. Gene expression array data from skeletal muscle and adipose tissue have provided some information about dysregulated metabolic pathways in women with PCOS, but the transcriptomic data need to be verified by proteomics to advance our understanding of PCOS. Skeletal muscle and adipose tissue biopsies from 10 women with PCOS and 10 controls were subjected to global proteomic analysis. Protein expression differences between cases and controls were based on Student’s t-test and corrected for multiple testing. In total, we identified 5000 proteins in adipose tissue and 3480 proteins in skeletal muscle. After correction for multiple testing, 74 proteins with q < 0.05 corresponding to 72 unique proteins were found to be differentially expressed in adipose tissue from women with PCOS versus controls. And, 123 proteins with q < 0.05 corresponding to 120 unique proteins were found to be differentially expressed in skeletal muscle from women with PCOS versus control. We then applied pathway analysis to the total protein and phosphopeptide data using PRISM and Enrichr.
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Project description:Subcutaneous adipose tissue gene expression profiles from women with PCOS, compared with age and BMI matched healthy controls (matched at group-level). A cross-section comparison was made between women with and without PCOS
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