MRNA expression data from skeletal muscle of type 2 diabetes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE18732 | GEO | 2010/01/19
SECONDARY ACCESSION(S): PRJNA121637
REPOSITORIES: GEO
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Project description:We used microarray technology to profile mRNA expression in the skeletal muscle of normal (NGT), glucose intolerant (IGT) and type 2 diabetic (DM) subjects. Groups were classified using WHO criteria and, importantly, the DM group were free of anti hypoglycaemic medication for one week prior to biopsy. Total RNA was extracted from the vastus lateralis of normal (NGT), glucose intolerant (IGT) and type 2 diabetic (DM) subjects (n = 118 in total) who had been free of hypoglycemic medication for one week. RNA was hybridized to Affymetric HGU133plus2 platform following manufacturer's directions.
2010-05-15 | E-GEOD-18732 | biostudies-arrayexpress
Project description:Global microRNA (miRNA) profiling was performed in 18 human islet donors using Exiqon’s LNA (locked nucleic acid)-based array platform. Donors were divided into three groups according to their HbA1c levels and type-2 diabetes diagnosis (normal glucose tolerance - NGT, impaired glucose tolerance - IGT, diagnosed with type-2 diabetes-T2D). To identify miRNAs with altered expression due to glyceamic status, donors were matched for age, gender and BMI and differential expression analysis was performed in 7 NGT vs 7 IGT/T2D donors using Significance Analysis of Microarrays (SAM) based on False Discovery Rate (FDR) statistics.
2022-02-28 | E-MTAB-11125 | biostudies-arrayexpress
Project description:People with diabetes are more likely to develop tuberculosis (TB) and to have poor TB treatment outcomes than those without. We previously showed that blood transcriptomes in people with TB-diabetes (TB-DM) co-morbidity have excessive inflammatory and reduced interferon responses at TB diagnosis. It is unknown whether this persists through treatment, potentially underlying adverse outcomes. Methods Pulmonary TB patients were recruited in South Africa, Indonesia and Romania, and classified as having TB-DM, TB with prediabetes, TB-related hyperglycaemia or uncomplicated TB, based on glycated haemoglobin (HbA1c) concentration at TB diagnosis and after 6 months of TB treatment. Gene expression in blood samples collected at diagnosis and at regular intervals throughout treatment was measured by unbiased RNA-Seq and targeted Multiplex Ligation-dependent Probe Amplification. Results Gene expression was modulated by TB treatment in all groups but to different extents, such that differences remained in people with TB-DM relative to TB-only throughout, including genes involved in innate responses, anti-microbial immunity and the inflammasome. People with prediabetes or with TB-related hyperglycaemia had gene expression more similar to people with TB-DM than TB-only throughout treatment. The overall pattern of change was similar across clinical groups irrespective of glycaemic index, permitting models predictive of TB treatment to be developed. Conclusions The exacerbated transcriptome changes seen in TB-DM take longer to resolve during TB treatment, indicating that prolonged treatment or host-directed therapy may be needed to improve TB treatment outcomes. Development of transcriptome-based biomarker signatures of TB-treatment response should include people with diabetes to be useful across populations.
2023-09-05 | GSE193978 | GEO
Project description:Type 2 diabetes mellitus (DM) is characterized by insulin resistance and pancreatic beta-cell dysfunction. In high-risk subjects, the earliest detectable abnormality is insulin resistance in skeletal muscle. Impaired insulin-mediated signaling, gene expression, and glycogen synthesis, and accumulation of intramyocellular triglycerides have all been linked with insulin resistance, but no specific defect responsible for insulin resistance and DM has been identified in humans. To identify genes potentially important in the pathogenesis of DM, we analyzed gene expression in skeletal muscle from healthy metabolically characterized nondiabetic (family history negative and positive for DM) and diabetic Mexican-American subjects. We demonstrate that insulin resistance and DM associate with reduced expression of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative metabolism and mitochondrial function. While NRF-1 expression is decreased only in diabetic subjects, expression of both PPARg coactivator 1-alpha and -beta (PGC1-a/PPARGC1, and PGC1-b/PERC), coactivators of NRF-1 and PPARg-dependent transcription, is decreased in both diabetic subjects and family history positive nondiabetic subjects. Decreased PGC1 expression may be responsible for decreased expression of NRFdependent genes, leading to the metabolic disturbances characteristic of insulin resistance and DM. Human muscle samples were obtained from five subjects with type 2 diabetes and ten subjects without diabetes, as well as 5 aliquots from a single subject without diabetes. The subjects without diabetes were further classified as family history positive (four subjects) or family history negative (six subjects).
2010-04-27 | E-GEOD-21340 | biostudies-arrayexpress
Project description:The microRNA (miRNA) expression profile of plasma exosome in pregnant women complicated with gestational diabetes mellitus (GDM) has not been fully clarified. In this study, differentially expressed miRNAs in plasma exosomes were identified by high-throughput small RNA sequencing in 12 GDM and 12 normal glucose tolerance (NGT) pregnant women and validated in 102 GDM and 101 NGT pregnant women. A total of 22 exosomal miRNAs were found and five of them were verified by qRT-PCR. Exosomal miR-423-5p was upregulated, while miR-99a-5p, miR-192-5p, miR-148a-3p, and miR-122-5p were downregulated in pregnant women complicated with GDM.
2022-11-09 | GSE192813 | GEO
Project description:Background: Diabetes mellitus (DM) is a recognized risk factor for dementias, including AD, increasing its odds by two-fold. Because DM is potentially modifiable risk factor, a greater understanding of the mechanisms linking DM to the clinical expression of AD may provide insights into much needed dementia therapeutics. Epigenetics offers a novel approach, and previously under-investigated 5-hydroxymethylcytosines (5hmC) is now emerging as a promising measure to investigate in diabetes related conditions. Methods: Using 5hmC-Seal, a highly sensitive chemical labeling technique developed by our team, we performed genome-wide profiling of 5hmC in circulating cell-free DNA (cfDNA) and prefrontal cortex tissue from 80 individuals across four groups: AD, DM, DM and AD (AD+DM), and non-AD/non-DM controls. We used differential analysis and machine-learning to explore whether 5hmC and biological pathways might be implicated in DM-associated AD under a balanced design. Results: We uncovered distinct 5hmC genome-wide signatures and biological pathways associated with AD or AD+DM compared to non-AD/non-DM controls or DM alone. We further demonstrated potential diagnostic value of 5hmC profiling in circulating cfDNA through feature selection based on machine learning. Conclusions: Genome-wide 5hmC profiling uncovered genomic features and biological pathways linking DM to DM-associated AD. Our findings also demonstrate the potential of utilizing 5hmC in circulating cfDNA as diagnostic biomarkers or disease monitoring tools, with the ultimate goal of preventing or ameliorating DM-associated AD dementia and improving clinical outcomes.
2023-05-16 | GSE203337 | GEO
Project description:Puberty unmasks or accelerates nephropathies, including the nephropathy of diabetes mellitus (DM). A number of cellular systems implicated in the kidney disease of DM interweave, forming an interdependent functional web. We performed focused microarray analysis to test the hypothesis that one or more genes in the transforming growth factor beta (TGF-β) signaling system would be differentially regulated in male rats depending on the age of onset of DM. Keywords: Age-Disease State Interaction Analysis
2007-09-30 | GSE7253 | GEO
Project description:<p>Pulmonary tuberculosis (PTB) and diabetes mellitus (DM) are common chronic diseases that threaten human health. Patients with DM are susceptible to PTB, an important factor that aggravates the complications of diabetes. However, the molecular regulatory mechanism underlying the susceptibility of patients with DM to PTB infection remains unknown. Healthy subjects, patients with primary PTB and patients with primary PTB complicated by DM were recruited according to inclusion and exclusion criteria. Peripheral whole blood was collected, and alteration profiles and potential molecular mechanisms were further analyzed using integrated bioinformatics analysis of metabolomics and transcriptomics. In this study, transcriptional data revealed that lipocalin 2 (LCN2), defensin alpha 1 (DEFA1), peptidoglycan recognition protein 1 (PGLYRP1) and integrin subunit alpha 2b (ITGA2B) were significantly upregulated, while chloride intracellular channel 3 (CLIC3) significantly down-regulated in PTB-DM by contrast to HC group. Additionally, the IL-17, PI3K-AKT and PPAR signaling pathways are important for PTB infection and regulation of PTB-complicated diabetes. Metabolomic data showed that glycerophospholipid metabolism, carbon metabolism and fat digestion and absorption processes were enriched in the differential metabolic analysis. Finally, integrated analysis of both metabolomic and transcriptomic data indicated that the NOTCH1/JAK/STAT signaling pathway is important in PTB complicated by DM. In conclusion, PTB infection altered the transcriptional and metabolic profiles of patients with DM. Metabolomic and transcriptomic changes were highly correlated in PTB-infected patients with DM. Peripheral metabolite levels may be used as biomarkers for PTB management in patients with DM.</p><p><strong>IMPORTANCE:</strong> The comorbidity of diabetes mellitus (DM) significantly increases the risk of tuberculosis infection and adverse tuberculosis treatment outcomes. Most previous studies have focused on the relationship between the effect of blood glucose control and the outcome of anti-tuberculosis treatment in pulmonary tuberculosis (PTB)-DM; however, early prediction and the underlying molecular mechanism of susceptibility to PTB infection in patients with DM remain unclear. Here, transcriptome sequencing and untargeted metabolomics were performed to elucidatethe key molecules and signaling pathways involved in PTB infection and the susceptibility of patients with diabetes to PTB. Our findings contribute to the development of vital diagnostic biomarkers for PTB or PTB-DM and provide acomprehensive understanding of molecular regulation during disease progression.</p>
2023-07-26 | MTBLS7623 | MetaboLights
Project description:Skeletal muscle is a primary tissue responsible for both the exercise capacity and insulin-induced glucose uptake. Exercise-evoked proteomic alternations in muscle of subjects with prediabetes are of great importance for the elucidation of the connections between insulin resistance and physical exercise. To envision best aviable approach, we compared various ion-chromatogram libraries assembled with the use of off-line high-pH fractionation (HpH), gas-phase fractionation (GPF) and library-less DirectDIATM approach in LC/MS/HRMS DIA proteomic analysis of muscle from normoglycemic (NGT) and prediabetic (IGT) subjects after 3 months of supervised, mixed-mode exercise. Although HpH approach to library generation resulted in best proteome coverage, quantitative and qualitative analysis of HeLa standards, mixed samples and whole study set revealed, that GPF-fractionated hybrid DDA/DIA-acquired libraries yielded best overall balance between the speed of preparation, data collection, data analysis and identification in real-life clinical samples.
2025-07-22 | PXD055536 | Pride
Project description:The goal of the project is to understand the mitochondrial proteome profiles related to T2DM. We performed comprehensive proteome profiling of mitochondria isolated from skeletal muscles in nine T2DM patients and nine control subjects with normal glucose tolerance (NGT).
2018-10-02 | PXD004312 | Pride