Roxadustat alleviates metabolic traits in letrozole-induced PCOS mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1086453 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28288618_1.fastq.gz | Fastqsanger.gz | |||
| SRR28288618_2.fastq.gz | Fastqsanger.gz | |||
| SRR28288619_1.fastq.gz | Fastqsanger.gz | |||
| SRR28288619_2.fastq.gz | Fastqsanger.gz | |||
| SRR28288620_1.fastq.gz | Fastqsanger.gz |
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Project description:Polycystic ovary syndrome (PCOS) is a heterogeneous condition, of polyhedric pathogenesis and clinical presentation, defined by oligo-/anovulation, hyperandrogenism and/or polycystic ovaries. Metabolic complications are highly common also in patients suffering PCOS, including obesity, insulin resistance and type-2 diabetes, which severely compromise the clinical course of affected women. Yet, therapeutic options for PCOS remain mostly symptomatic and of limited efficacy for improving both metabolic and reproductive alterations. We report herein the hormonal, metabolic and gonadal responses to different GLP1-based multi-agonists, namely GLP1/Estrogen (GLP1/E), GLP1/GIP and GLP1/GIP/Glucagon, in two murine models of PCOS, with variable penetrance of metabolic and reproductive traits, and their comparison with metformin. Our data illustrate the superior efficacy of the di-agonist, GLP1/E, vs. other multi-agonists and metformin in the management of the metabolic complications of PCOS; GLP1/E was able to ameliorate also ovarian cyclicity in an ovulatory model of PCOS, without direct estrogenic uterotrophic effects. In keeping with GLP1-mediated brain targeting, label-free, quantitative proteomics revealed changes in common and distinct hypothalamic pathways in response to GLP1/E between the two PCOS models, as basis for differential efficiency. Altogether, our data set the basis for the use of GLP1-based multi-agonists, and particularly GLP1/E, in the personalized management of PCOS.
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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: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-1α 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. Keywords: PCOS, microarray, global pathway analysis, insulin resistance, pioglitazone, protein metabolism, mitochondrial oxidative metabolism
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