Ontology highlight
ABSTRACT:
PROVIDER: PRJNA655811 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12407008.fastq.gz | Fastqsanger.gz | |||
| SRR12407009.fastq.gz | Fastqsanger.gz | |||
| SRR12407010.fastq.gz | Fastqsanger.gz |
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Project description:The study aimed to investigate molecular signatures in peripheral blood of individuals affected by metabolic syndrome (MetS) and different degrees of obesity. Metabolic health of 1204 individuals was assessed, and 32 subjects were recruited to four study groups: MetS lean, MetS obese, “healthy obese” and healthy lean. Whole-blood transcriptome next generation sequencing with functional data analysis was carried out.
2020-02-18 | GSE145412 | GEO
Project description:The metabolic syndrome (MetS) is characterized by the presence of metabolic abnormalities that include abdominal obesity, dyslipidemia, hypertension, increased blood glucose/insulin resistance, hypertriglyceridemia and increased risk for cardiovascular disease (CVD). The ApoE*3Leiden.human Cholesteryl Ester Transfer Protein (ApoE3L.CETP) mouse model manifests several features of the MetS upon high fat diet (HFD) feeding. Moreover, the physiological changes in the white adipose tissue (WAT) contribute to MetS comorbidities. The aim of this study was to identify transcriptomic signatures in the gonadal WAT of ApoE3L.CETP mice in discrete stages of diet-induced MetS.
2020-07-14 | GSE139601 | GEO
Project description:The metabolic syndrome (MetS) is attributed to a number of risk factors related to obesity and its comorbidities such as hypertension, increased blood glucose, hypertriglyceridemia and cardiovascular disease (CAD). Several mouse models have been used trying to understand the metabolic abnormalities occur in obesity and MetS. However, The ApoE*3Leiden.human Cholesteryl Ester Transfer Protein (ApoE3L.CETP) mouse model better describes the physiology and pathophysiology of the MetS upon high fat diet (HFD) feeding. Towards MetS treatment, Roux-en-Y gastric bypass (RYGB) is a surgical bariatric approach that allows to achieve sustained and long-term weight loss and to improve comorbidities of the MetS. The aim of this study was to elucidate whether improvements in lipid and glucose metabolism after RYGB surgery are body weight-dependent or not and to identify transcriptomic signatures related to these phenotypic observations.
2019-07-05 | GSE125946 | GEO
Project description:The metabolic syndrome (MetS), a collective cluster of disease risk factors that includes dyslipidemia, obesity, inflammation, hypertension, and insulin resistance, affects numerous people worldwide. Accumulating studies have shown that long-noncoding RNAs (lncRNA) serve as competing endogenous RNA (ceRNA) to play essential roles in regulating gene expression in various diseases. To explore the role of lncRNAs as ceRNAs in MetS, we examined a MetS-associated network in circulating extracellular vesicles (EVs) collected from systemic blood of MetS and control patients (n=5 each). MetS patients showed elevated body-weight, glucose, blood pressure, insulin, liver injury and inflammatory markers levels. In total, 191 differentially-expressed (DE) lncRNAs, 1389 mRNAs, and 138 miRNAs were selected for further analysis. Biological processes and pathway functional enrichment analysis were performed based on the Database for Annotation, Visualization, and Integrated Discovery (DAVID) database. LncRNA/mRNA/miRNA ceRNA network was constructed by Cytoscape v3.8 based on the DE-RNAs, and included 13 lncRNAs, 8 miRNAs, and 64 mRNAs. We found that the lncRNA-associated ceRNA network members potentially serve as regulators of central cellular processes and complications of MetS, including cancer. These findings suggest that MetS alters the interactions among the ceRNA network components in circulating EV-specific ceRNA network, and implicate the cargo of circulating EVs in ramifications of MetS.
2021-02-10 | GSE166474 | GEO
Project description:The metabolic syndrome (MetS) is a collection of co-occurring complex disorders including obesity, hypertension, dyslipidemia, and insulin resistance. The Lyon Hypertensive (LH) and Lyon Normotensive (LN) rats are models of MetS sensitivity and resistance, respectively. To identify genetic determinants and mechanisms underlying MetS, 169 rats from an F2 intercross between LH and LN were studied. Multi-dimensional data were obtained including genotypes of 1536 SNPs, 23 physiological traits including blood pressure, plasma lipid and leptin levels, and body weight/adiposity, and more than 150 billion nucleotides of RNA-seq reads from the livers of 36 F2 individuals, 6 LH and 6 LN individuals. We identified 17 pQTLs (physiological quantitative trait loci) and 1200 eQTLs (gene expression quantitative trait loci). Systems biology methods were applied to identify 18 candidate MetS genes, including genes (Prcp and Aqp11) previously shown to be MetS-related. We found an eQTL hotspot on RNO17, which was also located within pQTLs for MetS-related traits. The genes regulated by this eQTL hotspot were mainly in two co-expression network modules (a mitochondria related module and a gene regulation related module) and were predicted to causally affect many MetS-related traits. Multiple evidences strongly and consistently support RGD1562963, a gene regulated in cis by this eQTL hotspot and possibly related to RNA stability, as the eQTL driver gene directly affected by genetic variation between LH and LN rats; the expression of this gene is also correlated with MetS-related traits. Our study sheds light on the intricate pathogenesis of MetS and proved that systems biology with high-throughput sequencing is a powerful method to study the etiology of complicated diseases. RNA-Seq of the liver of 6 LH (Lyon Hypertensive) rats and 6 LN (Lyon Normotensive) rats and 36 F2 rats.
2014-10-31 | E-GEOD-50027 | biostudies-arrayexpress
Project description:Metabolic syndrome (MetS), a cluster of metabolic abnormalities that occur concurrently that significantly increases the risk of cardiovascular disease and mortality. 3-mercaptopyruvate sulfurtransferase (MPST), a cysteine-catabolizing enzyme that yields pyruvate and hydrogen sulfide (H2S), plays a central role in the regulation of energy homeostasis. Herein, we seek to investigate the role of MPST/H2S in MetS using a mouse model of the disease.Wilt type (WT) mice were fed a high-fat diet (HFD) for 15 weeks to induce obesity and hyperglycemia, and followed by a nitric oxide synthase inhibitor, for the additional 5 weeks to induce hypertension and MetS. This MetS mouse model caused a mild diastolic and endothelial dysfunction. We observed that, MetS was characterized by decreased levels of free H2S and sulfane-sulfur and downregulation of MPST in the aorta of animals with MetS. Global deletion of Mpst (Mpst-/-) results in increased body weight and greater glucose intolerance in mice with MetS, without affecting their blood pressure. Whole transcriptome analysis in aortic tissue revealed an upregulation of genes involved in the immune response; CD8+ cell infiltration and T-cell activation-related pathways were observed among the most affected biological processes in Mpst-/- mice with MetS.
2024-12-23 | GSE273901 | GEO
Project description:To identify distinctive miRNA signatures in OSAHS with Mets patients from healthy subjects, that could serve as diagnostic biomarkers or describe differential molecular mechanisms with potential therapeutic implications. 5 OSAHS with metabolic syndrome (MetS) patients and 4 Tibetan healthy subjects were selected as the control group from January 2018 to January 2021, who signed an informed, written consent form. All OSAHS Patients diagnosed by Polysomnography (PSG). Patients suffering from other respiratory diseases, or combined with allergic and autoimmune diseases, tumors and other serious systemic serious primary diseases were excluded from this study. Plasma was isolated and frozen at -80 ◦C.
2025-01-29 | GSE274563 | GEO
Project description:Clinical studies have demonstrated that higher protein intake based on caloric restriction (CR) alleviates metabolic abnormalities. However, no study has examined the effects of plasma protein profiles on caloric restriction with protein supplementation (CRPS) in metabolic syndrome (MetS). Therefore, using a proteomic perspective, this pilot study investigated whether CRPS ameliorated metabolic abnormalities associated with MetS in middle-aged women. Methods: Plasma samples of middle-aged women with MetS in CR and CRPS groups for 12-week intervention were obtained and their protein profiles were analysed. Briefly, blood samples from qualified participants were drawn before and after the dietary treatment. Anthropometric, clinical, and biochemical variables were measured and correlated with plasma proteomics. Results: In results, we found that body mass index, total body fat, and fasting blood glucose decreased significantly after the interventions but were not different between the CR and CRPS groups. After liquid chromatography–tandem mass spectrometry analysis, the relative plasma levels of A2M, C4BPA, C1RL, C6, C8G, and PROS were significantly different between the CRPS and CR groups. These proteins are involved in inflammation, the immune system, and coagulation responses. Moreover, blood low-density lipoprotein cholesterol levels were significantly and positively correlated with C6 plasma levels in both groups. Conclusions: These findings suggest that CRPS improves inflammatory responses in middle-aged women with MetS. Specific plasma protein expression (i.e. A2M, C4BPA, C1RL, C6, C8G, and PROS) associated with the complement system was highly correlated with FBG, BLs, and body fat.
2019-11-13 | PXD012213 | Pride
Project description:Background and Aims Within the next decade, non-alcoholic fatty liver disease (NAFLD) is predicted to become the most prevalent cause of childhood liver failure in developed countries. Predisposition to juvenile NAFLD can be programmed during early life in response to maternal metabolic syndrome (MetS), but the underlying mechanisms are poorly understood. We hypothesized that imprinted genes, defined by expression from a single parental allele, play a key role in maternal MetS-induced NAFLD, due to their susceptibility to environmental stressors and their functions in liver homeostasis. We aimed to test this hypothesis and determine the critical periods of susceptibility to maternal MetS. Approach and Results We established a mouse model to compare the effects of MetS during prenatal and postnatal development on NAFLD. Postnatal but not prenatal MetS exposure is associated with histological, biochemical and molecular signatures of hepatic steatosis and fibrosis in juvenile mice. Using RNA-seq, we show that the Imprinted Gene Network (IGN), including its regulator Zac1, is up-regulated and over-represented among differentially expressed genes, consistent with a role in maternal MetS-induced NAFLD. In support of this, activation of the IGN in cultured hepatoma cells by over-expressing Zac1 is sufficient to induce signatures of profibrogenic transformation. Using chromatin immunoprecipitation, we demonstrate that Zac1 binds the TGF-β1 and COL6A2 promoters, forming a direct pathway between imprinted genes and well-characterized pathophysiological mechanisms of NAFLD. Finally, we show that hepatocyte-specific over-expression of Zac1 is sufficient to drive fibrosis in vivo. Conclusions Our findings identify a novel pathway linking maternal MetS exposure during postnatal development to the programming of juvenile NAFLD, and provide support for the hypothesis that imprinted genes play a central role in metabolic disease programming.
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