Project description:Why ~70% of women with polycystic ovary syndrome (PCOS) have intrinsic insulin resistance (IR), above and beyond that associated with body mass, including dysfunctional glucose metabolism in adipose tissue (AT), remains a fundamental question. In these experiments, we sought to explore the role of miRNAs in the AT of PCOS and matched controls. Analysis determined that PCOS AT has a differentially expressed miRNA profile, including upregulated miR-93. We observed a significant association between HOMA-IR, and GLUT4 and miR-93 expression in human AT. Our results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93, and demonstrate upregulated miR-93 expression in PCOS, possibly accounting for the IR of the syndrome, and also in non-PCOS women with IR. We performed miRNA microarrays to determine PCOS-related miRNA expression in adipose derived from lean PCOS patients and matched control women. We analyized miRNA from total RNA extracted from subcutaneous (sc) adipose tissue from three lean PCOS patients and three matched control women.
Project description:In previous studies, multiple animal models (rhesus monkeys, sheep) have suggested a developmental programming effect of PCOS. The goal of this study was to examine whether developmental programming may accompany epigenetic changes by examining intrinsic epigenetic differences, specifically chromatin accessibility, in adipose stem cells (ASCs) from subcutaneous (SC) adipose tissue of PCOS women vs age- and BMI-matched control samples as they mature into adipocytes in vitro.
Project description:Why ~70% of women with polycystic ovary syndrome (PCOS) have intrinsic insulin resistance (IR), above and beyond that associated with body mass, including dysfunctional glucose metabolism in adipose tissue (AT), remains a fundamental question. In these experiments, we sought to explore the role of miRNAs in the AT of PCOS and matched controls. Analysis determined that PCOS AT has a differentially expressed miRNA profile, including upregulated miR-93. We observed a significant association between HOMA-IR, and GLUT4 and miR-93 expression in human AT. Our results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93, and demonstrate upregulated miR-93 expression in PCOS, possibly accounting for the IR of the syndrome, and also in non-PCOS women with IR. We performed miRNA microarrays to determine PCOS-related miRNA expression in adipose derived from lean PCOS patients and matched control women.
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
Project description:Subcutaneous adipose tissue gene expression profiles from women with PCOS, compared with age and BMI matched healthy controls (matched at group-level).
Project description:Objective: The etiology of PCOS is mostly unknown. Existing data support both genetic and environmental factors in its pathogenesis. Design: Prospective case - control study. Setting: University Hospital. Patients: 25 patients undergoing IVF-ICSI treatment. Intervention: Genome-wide oligonucleotide microarray technology was used to study differential gene-expression patterns of cultured human cumulus cells from IVF patients divided into 4 groups according to disease state (PCOS vs. Control) and BMI (Obese vs. Lean). Results: Two differential PCOS gene expression profiles were established: Lean-Type was formed by comparing PCOS lean (PL) vs. non-PCOS lean (NL) individuals; Obese-Type was formed by comparing PCOS obese (PO) vs. non-PCOS (NO) obese patients. Conclusions: Different molecular pathways are associated with PCOS in Lean and Obese individuals, as demonstrated by gene expression profiling of cumulus cells. Our findings provide insights into the molecular pathogenesis of PCOS. We used microarrays to study the gene expression of human cultured cumulus cells. We compared the genes expression of lean PCOS, Obese PCOS, lean controls and obese controls. Different molecular pathways are associated with PCOS in Lean and Obese patients. Keywords: disease state analysis
Project description:Objective: The etiology of PCOS is mostly unknown. Existing data support both genetic and environmental factors in its pathogenesis. Design: Prospective case - control study. Setting: University Hospital. Patients: 25 patients undergoing IVF-ICSI treatment. Intervention: Genome-wide oligonucleotide microarray technology was used to study differential gene-expression patterns of cultured human cumulus cells from IVF patients divided into 4 groups according to disease state (PCOS vs. Control) and BMI (Obese vs. Lean). Results: Two differential PCOS gene expression profiles were established: Lean-Type was formed by comparing PCOS lean (PL) vs. non-PCOS lean (NL) individuals; Obese-Type was formed by comparing PCOS obese (PO) vs. non-PCOS (NO) obese patients. Conclusions: Different molecular pathways are associated with PCOS in Lean and Obese individuals, as demonstrated by gene expression profiling of cumulus cells. Our findings provide insights into the molecular pathogenesis of PCOS. We used microarrays to study the gene expression of human cultured cumulus cells. We compared the genes expression of lean PCOS, Obese PCOS, lean controls and obese controls. Different molecular pathways are associated with PCOS in Lean and Obese patients. Experiment Overall Design: Cumulus cells obtained from woman undergoing IVF/ICSI. Following oocyte retrieval, cumulus cells were stripped from the oocyte, in preparation for the ICSI process, with a micropipette. After 48h in culture the cumulus cells were collected for RNA extraction and hybridization on Affymetrix microarrays. We compered the expression profile of 4 groups - lean PCOS, obese PCOS, lean controls and obese controls.
Project description:Lean polycystic ovary syndrome (PCOS) women have a greater proportion of android (abdominal) fat, increased numbers of small subcutaneous (SC) abdominal adipocytes and preferential intra-abdominal fat accumulation. This study examines whether abnormal gene expression of SC abdominal adipose stem cells (ASCs) from lean PCOS women underlies this altered abdominal adipose structure-function. In this dataset, we include the expression data obtained from PCOS and NL subcutaneous adipose tissue. Differential expression of at least 1.5-fold change (P<0.05) were obtained in 120 genes (48 upregulated, 72 downregulated) of SC abdominal ASCs from PCOS versus NL women
Project description:Polycystic ovary syndrome (PCOS) is the most common endocrinological disorder of fertile-aged women. PCOS has been associated with adverse pregnancy outcomes and abnormalities of the placenta. By taking a quantitative label-free quantitative proteomics approach we set out to investigate if changes in the plasma proteome of pregnant women with PCOS could elucidate the mechanisms behind the pathologies observed in PCOS pregnancies. We have performed label-free quantitative proteomics on plasma samples from pregnant women with PCOS at term (n=14) and plasma samples from pregnant control women (n = 23) matched for age, gestational length and BMI. The samples are derived from BASIC pregnancy cohort from Uppsala, Sweden. A total of 169 proteins with two or more unique peptides were identified.
Project description:Adipocytes isolated from lean and obese postmenopausal women with no significant differences in metabolic syndrome parameters demonstrate changes in multiple inflammatory, metabolic and structural gene families. Purified adipocyte samples were isolated from subcutaneous adipose tissue surgical biopsies of 7 obese (BMI>30) and 7 lean (BMI<25) postmenoposal women and gene expression was quantified with Agilent-014850, 4X44K human whole genome platform arrays (GPL6480)