Investigation of prodromal features in metabolic syndrome based on transcriptome analysis
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE200744 | GEO | 2023/04/01
REPOSITORIES: GEO
Similar Datasets
Project description: Not available
| S-EPMC10308104 | biostudies-literature
Project description:Investigation of prodromal features in metabolic syndrome based on transcriptome analysis
| PRJNA826462 | ENA
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:Metabolic syndrome is a common and complicated metabolic disorder and defined as a clustering of metabolic risk factors such as insulin resistance or diabetes, obesity, hypertension, and hyperlipidemia. The identification of accurate and effective biomarkers is beneficial to the early diagnosis and treatment of metabolic syndrome. Our study firstly detected the plasma miRNA expression profile of MetS patients compared with control group by high-throughput sequencing and integrated bioinformatics approaches. To our best knowledge, our study firstly perform high-throughput sequencing to obtain the circulating microRNA expression data in MetS plasma, and identified several potential plasma biomarkers for MetS.
2023-07-24 | GSE155096 | 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: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
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:Evaluate differences in gene methylation levels between obese men with and without the metabolic syndrome Visceral adipose tissue from obese men with the metabolic syndrome (MetS+, N=7) vs. obese men without the metabolic syndrome (MetS-, N=7)
2014-02-07 | E-GEOD-54776 | 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:Metabolic syndrome (MetS) is the name of cluster of risk factors that increases the risk for heart disease and other health problems by which several organs are affected, but research is lacking for those not involved directly in metabolism. The cluster is integrated by central obesity, insulin resistance, dyslipidemia (elevated triglycerides and low density lipoprotein and decreased high density lipoprotein), and high blood pressure, according to the consensus released by the International Diabetes Federation [1]. This problem could be as the result of an unbalanced diets (high-fat and carbohydrates), and genetic background [2, 3]. There is evidence that suggests that MetS is a condition that increases the risk of different lung diseases. It have been reported in some MetS patients a diminished lung function, as assessed by spirometry, in addition, there is an association with insulin resistance, increase in body mass index; abdominal obesity and systemic inflammation (high levels of C reactive protein) [4-6]. In other cases, like asthma, some components of MetS such as abdominal obesity, hypertension and pro-inflammatory cytokines have been with related with this disease [7-9]. Also, a few clinical studies reported that abdominal obesity, hyperglycemia and elevated levels of systemic inflammatory markers, which are components of MetS, were significantly more prevalent in patients with chronic obstructive pulmonary disease [10-13]. In the present work we evaluated the transcriptomic changes of lung tissue in an animal model of MetS induced by diet.
2017-07-01 | GSE73910 | GEO