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A transcriptomic analysis of a Caucasian family cohort of high risks for the metabolic syndrome [HumanWG-6 v3.0]

ABSTRACT: Metabolic Syndrome (MetS) is a strong predictor for diabetes and cardiovascular disease and is defined by a constellation of phenotypes including increased and adverse body fat distribution, insulin resistance, abnormalities in lipids and lipoproteins, malfunctional cardiovascular performance, and abnormal levels of adipokines and cytokines. We assayed in a subset of our family cohort phentoyped for MetS phentoypes, the genome-wde transcript levels using the Illumina Human WG-6 v3 expression arrays.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45986 | GEO | 2013/04/12

SECONDARY ACCESSION(S): PRJNA196836

REPOSITORIES: GEO

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A transcriptomic analysis of a Caucasian family cohort of high risks for the metabolic syndrome [HumanWG-6 v3.0]

Project description:Metabolic Syndrome (MetS) is a strong predictor for diabetes and cardiovascular disease and is defined by a constellation of phenotypes including increased and adverse body fat distribution, insulin resistance, abnormalities in lipids and lipoproteins, malfunctional cardiovascular performance, and abnormal levels of adipokines and cytokines. We assayed in a subset of our family cohort phentoyped for MetS phentoypes, the genome-wde transcript levels using the Illumina Human WG-6 v3 expression arrays. Genome-wide gene expression was assayed in members of families that originally contribute to linkage signals in a previous genome-wide linkage scans for multiple MetS phenotypes.

2013-04-12 | E-GEOD-45986 | biostudies-arrayexpress

A transcriptomic analysis of a Caucasian family cohort of high risks for the metabolic syndrome [HumanWG-6 v2.0]

2013-04-05 | GSE45792 | GEO

A transcriptomic analysis of a Caucasian family cohort of high risks for the metabolic syndrome [HumanWG-6 v2.0]

Project description:Metabolic Syndrome (MetS) is a strong predictor for diabetes and cardiovascular disease and is defined by a constellation of phenotypes including increased and adverse body fat distribution, insulin resistance, abnormalities in lipids and lipoproteins, malfunctional cardiovascular performance, and abnormal levels of adipokines and cytokines. We assayed in a subset of our family cohort phentoyped for MetS phentoypes, the genome-wde transcript levels using the Illumina Human WG-6 v2 expression arrays. Genome-wide gene expression was assayed in members of families that originally contribute to linkage signals in a previous genome-wide linkage scans for multiple MetS phenotypes.

2013-04-05 | E-GEOD-45792 | biostudies-arrayexpress

Cyclodextrin protects podocytes in diabetic kidney disease [HumanWG-6 v3.0 array]

Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C).

2013-07-11 | GSE46897 | GEO

Cardiac Remodeling During Pregnancy With Metabolic Syndrome: Prologue of Pathological Remodeling

Project description:The heart undergoes physiological hypertrophy during pregnancy in healthy individuals. Metabolic syndrome (MetS) is now prevalent in women of child-bearing age and might add risks of adverse cardiovascular events during pregnancy. The present study asks if cardiac remodeling during pregnancy in obese individuals with MetS is abnormal and whether this predisposes them to a higher risk for cardiovascular disorders. The idea that MetS induces pathological cardiac remodeling during pregnancy was studied in a long-term (15 weeks) Western diet–feeding animal model that recapitulated features of human MetS. Pregnant female mice with Western diet (45% kcal fat)–induced MetS were compared with pregnant and nonpregnant females fed a control diet (10% kcal fat). Pregnant mice fed a Western diet had increased heart mass and exhibited key features of pathological hypertrophy, including fibrosis and upregulation of fetal genes associated with pathological hypertrophy. Hearts from pregnant animals with WD-induced MetS had a distinct gene expression profile that could underlie their pathological remodeling. Concurrently, pregnant female mice with MetS showed more severe cardiac hypertrophy and exacerbated cardiac dysfunction when challenged with angiotensin II/phenylephrine infusion after delivery. These results suggest that preexisting MetS could disrupt physiological hypertrophy during pregnancy to produce pathological cardiac remodeling that could predispose the heart to chronic disorders.

2023-07-13 | GSE237063 | GEO

Transcriptomic profiling of the white adipose tissue (WAT) in ApoE3L.CETP mice fed a high fat diet (HFD) or a low fat diet (LFD) for three different time periods, or chow diet at baseline

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

Cyclodextrin protects podocytes in diabetic kidney disease [HumanWG-6 v3.0 array]

2013-07-11 | E-GEOD-46897 | biostudies-arrayexpress

Characteristics of Cross-Hybridization and Cross-Alignment in Pseudo-Xenograft samples by RNA-Seq and Microarrays [Illumina HumanWG-6 v3.0]

Project description: Not available

| S-ECPF-GEOD-40866 | biostudies-other

Transcriptomic profiling of the liver after Roux-en-Y gastric bypass in a humanized murine model of the metabolic syndrome

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

Influenza Vaccines Differentially Regulate the Interferon Response in Human Dendritic Cell Subsets [HumanWG-6 v3.0 Beadchip Experiments]

Project description:Human dendritic cells play a fundamental role in the initiation of long-term adaptive immunity during vaccination against influenza. Understanding the early response of human DCs to vaccine challenge is thus essential to determine the nature and magnitude of maturation signals that strongly correlate with vaccine effectiveness. Here, we show that the non-adjuvanted trivalent Fluzone®09-10 (TIV-09) induces monocyte-derived DCs (moDCs), purified blood conventional DCs (cDCs) and plasmacytoid DCs (pDCs) to express CD80, CD83, and CD86, and secrete cytokines. TIV-09 stimulated the secretion of type I interferons (IFN) IFN-α and IFN-β and type III IFN IL-29 by moDCs and cDCs subsets. The vaccine also induced the production of IL-6, TNF and the chemokines IP-10 and MIP-1β. Conversely, the non-adjuvanted monovalent H1N1 California vaccine (MIV-09), which was commercialized in 2009 during the H1N1 epidemics and displayed lower effectiveness in retrospective studies, did not induce the production of type I IFN in moDCs and blood cDCs. Furthermore, it inhibited the TIV-09-induced secretion of type I IFN by these DCs. Yet, both vaccines induced pDCs to secrete type I IFN indicating that different influenza vaccines activate different molecular signaling pathways in different DC subsets. In vivo, the baseline IFN signature was decreased upon administration of the H1N1 vaccine in 3/3 pediatric lupus patients. These results suggest that subtypes of non-adjuvanted influenza vaccines elicit long-term protection through different mechanisms and that a vaccine’s ability to induce an IFN response in DCs may palliate the absence of adjuvant and increase vaccine efficacy.

2016-12-25 | GSE81690 | GEO

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