E-MTAB-3017
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ABSTRACT:
PROVIDER: E-MTAB-3017 | ExpressionAtlas | 2014-11-21
REPOSITORIES: ExpressionAtlas
Similar Datasets
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: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:Context: It is not known whether biological differences reported between subcutaneous (SAT) and visceral (VAT) adipose tissue depots underlie the pathogenicity of visceral fat. Objective: We compared SAT and VAT gene expression according to obesity, visceral fat accumulation, insulin resistance and presence of the metabolic syndrome. Design: Subjects were assigned into 4 groups (lean, overweight, obese and obese with metabolic syndrome). Setting: Subjects were recruited at a university hospital. Patients: 32 women were included. Main Outcome Measures: Anthropometric measurements, euglycemic hyperinsulinemic clamps, blood analyses and computed tomography scans were performed and paired samples of SAT and VAT were obtained for DNA microarray-based gene expression profiling.
2010-12-07 | GSE24883 | GEO
Project description:We investigated the effect of pterocarpan-rich extract from soybean leaf on metabolic syndrome and elucidated anti-inflammation mechanism based on RNA-seq transcriptomic profiles in overweight and obese subjects
2017-02-09 | GSE80714 | GEO
Project description:Objectives: We compared metabolic biomarkers in the blood and PBMC gene expression profiles among normal weight, mildly obese, and moderately obese Korean adult men. Design: Subjects were classified as normal weight (BMI, 18.5~23 kg/m2), mildly obese (BMI, 25~27.5 kg/m2), and moderately obese (BMI, 27.5~30 kg/m2). Results: High leptin, lipids (except LDL- and HDL-cholesterol), and apolipoprotein B levels and low adiponectin and HDL-cholesterol levels were present in the plasma of both mildly and moderately obese subjects. Circulating levels of inflammatory cytokines (TNF-α and IL-6) and markers of insulin resistance, oxidative stress, and liver damage were altered in moderately obese subjects but not mildly obese subjects. PBMC transcriptome data showed enrichment of pathways involved in energy metabolism, insulin resistance, bone metabolism, cancer, inflammation, and fibrosis in both mildly and moderately obese subjects. Signaling pathways involved in oxidative phosphorylation; triglyceride synthesis; carbohydrate metabolism; insulin, mTOR, FOXO, RAP1, RAS, and TGF-β signaling; and ECM–receptor interaction were enriched only in moderately obese subjects, indicating that changes in PBMC gene expression profiles according to metabolic disturbances were associated with the development and/or aggravation of obesity. In particular, upregulation of 8 genes (FLT3LG, LTB, IL23A, CD19, CPT1B, AXIN2, CACNA1L, RPRM) and downregulation of 2 genes (CCL4L1, LPAR5) were observed only in mildly obese subjects. Six genes (CXCR5, NFKBIA, BIRC3, TNFAIP3, DDIT3, PDE4B) and 4 genes (CX3CR1, HSPA1A, CACNA2D3, APAF1) were up- and down-regulated, respectively, in both mildly and moderately obese subjects. These results suggested that these genes could be used as early or stable biomarkers for diagnosing and treating obesity-associated metabolic disturbance.
2018-05-01 | GSE69039 | GEO
Project description:Gene expression in peripheral blood is shown sufficient to differentiate patients with metabolic disorders from control. The signatures of metabolic syndrome, coronary artery disease and type 2 diabetes also have significant overlap. Microarrays were performed on 35 subjects in the following groups: control (n=9), rheumatoid arthritis (n=6), metabolic syndrome (n= 6), coronary artery disease (n=6) and type 2 diabetes (n=8). Intensity values for each array were normalized to a sum of 10,000.
2010-08-12 | E-GEOD-23561 | biostudies-arrayexpress
Project description:Metabolic syndrome, whose main diagnostic component is obesity, is a risk factor for lifestyle-related diseases, type 2 diabetes, and cardiovascular disease. Diet is known to affect the prevalence of metabolic syndrome. However, the effect of diet on metabolic syndrome in Japanese subjects has not been thoroughly explored. In the present study, we investigated the effect of carotenoid-rich vegetables, particularly lycopene- and lutein-rich vegetables, on the metabolic syndrome in obese Japanese men. We conducted an 8-week long randomized, double-blinded, controlled clinical trial in which, 28 middle-aged (40 ≤ age < 65) Japanese men with high body mass index (BMI ≥ 25) were randomized into four dietary groups: high lycopene + high lutein (HLyHLu), high lycopene + low lutein (HLyLLu), low lycopene + high lutein (LLyHLu), and low lycopene + low lutein (LLyLLu). Our results showed that daily beverage-intake increased the plasma levels of carotenoids without adverse effects, and the visceral fat level was significantly decreased in all the groups. The waist circumference was significantly decreased only in the HLyLLu group, whereas the CoQ10 oxidation rate was decreased in all the groups. The gene expression profiles of whole blood samples before and after ingestion differed only in the LLyLLu group, indicating the effect of carotenoids on gene expression profile. In conclusion, our results suggest that dietary uptake of carotenoids increases their concentration in blood, and reduces the intra-abdominal visceral fat.
2020-08-09 | GSE151683 | GEO
Project description:<p>Emerging evidence that the gut microbiota may contribute in important ways to human health and disease has led us and others to hypothesize that both symbiotic and pathological relationships between gut microbes and their host may be key contributors to obesity and the metabolic complications of obesity. Our "Thrifty Microbiome Hypothesis" poses that gut microbiota play a key role in human energy homeostasis. Specifically, constituents of the gut microbial community may introduce a survival advantage to its host in times of nutrient scarcity, promoting positive energy balance by increasing efficiency of nutrient absorption and improving metabolic efficiency and energy storage. However, in the presence of excess nutrients, fat accretion and obesity may result, and in genetically predisposed individuals, increased fat mass may result in preferential abdominal obesity, ectopic fat deposition (liver, muscle), and metabolic complications of obesity (insulin resistance, hypertension, hyperlipidemia). Furthermore, in the presence of excess nutrients, a pathological transition of the gut microbial community may occur, causing leakage of bacterial products into the intestinal lymphatics and portal circulation, thereby inducing an inflammatory state, further aggravating metabolic syndrome traits and accelerating atherosclerosis. This pathological transition and the extent to which antimicrobial leakage occurs and causes inflammatory and other maladaptive sequelae of obesity may also be influenced by host factors, including genetics. In the proposed study, we will directly test the Thrifty Microbiome Hypothesis by performing detailed genomic and functional assessment of gut microbial communities in intensively phenotyped and genotyped human subjects before and after intentional manipulation of the gut microbiome. To address these hypotheses, five specific aims are proposed: (1) enroll three age- and sex-matched groups from the Old Order Amish: (i) 50 obese subjects (BMI > 30 kg/m2) with metabolic syndrome, (ii) 50 obese subjects (BMI > 30 kg/m2) without metabolic syndrome, and (iii) 50 non-obese subjects (BMI < 25 kg/m2) without metabolic syndrome and characterize the architecture of the gut microbiota from the subjects enrolled in this study by high-throughput sequencing of 16S rRNA genes; (2) characterize the gene content (metagenome) to assess the metabolic potential of the gut microbiota in 75 subjects to determine whether particular genes or pathways are correlated with disease phenotype; (3) characterize the transcriptome in 75 subjects to determine whether differences in gene expression in the gut microbiota are correlated with disease phenotype, (4) determine the effect of manipulation of the gut microbiota with antibiotics on energy homeostasis, inflammation markers, and metabolic syndrome traits in 50 obese subjects with metabolic syndrome and (5) study the relationship between gut microbiota and metabolic and cardiovascular disease traits, weight change, and host genomics in 1,000 Amish already characterized for these traits and in whom 500K Affymetrix SNP chips have already been completed. These studies will provide our deepest understanding to date of the role of gut microbes in terms of 'who's there?', 'what are they doing?', and 'how are they influencing host energy homeostasis, obesity and its metabolic complications? PUBLIC HEALTH RELEVANCE: This study aims to unravel the contribution of the bacteria that normally inhabit the human gastrointestinal tract to the development of obesity, and its more severe metabolic consequences including cardiovascular disease, insulin resistance and Type II diabetes. We will take a multidisciplinary approach to study changes in the structure and function of gut microbial communities in three sets of Old Order Amish patients from Lancaster, Pennsylvania: obese patients, obese patients with metabolic syndrome and non-obese individuals. The Old Order Amish are a genetically closed homogeneous Caucasian population of Central European ancestry ideal for genetic studies. These works have the potential to provide new mechanistic insights into the role of gut microflora in obesity and metabolic syndrome, a disease that is responsible for significant morbidity in the adult population, and may ultimately lead to novel approaches for prevention and treatment of this disorder.</p>
| phs000258 | dbGaP
Project description:We investigated the effect of a saturated (SFA) and a monounsaturated (MUFA) rich diet on insulin sensitivity and adipose tissue gene expression profiles of subjects at risk for metabolic syndrome. A controlled-feeding trial was performed with 20 moderately overweight subjects. Subjects received a SFA-rich or a MUFA-rich diet for 8 weeks. Subcutaneous adipose tissue samples were obtained and insulin sensitivity was measured. Whole genome micro-array analysis was performed on the adipose tissue samples. Consumption of a SFA-rich diet resulted in a pro-inflammatory 'obese-like' gene expression profile while consumption of a MUFA-rich diet caused a more anti-inflammatory profile. This suggests that replacement of dietary SFA by MUFA could prevent adipose tissue inflammation and may reduce the risk for inflammation related diseases such as the metabolic syndrome.
2010-02-14 | GSE14954 | GEO
Project description:Evaluate differences in gene methylation levels between obese men with and without the metabolic syndrome
2014-02-07 | GSE54776 | GEO