Transcriptomic analysis of peripheral blood mononuclear cells (PBMC) of patients with type 2 Diabetes Melittus(T2DM), Dyslipidemia (DL) and Periodontitis (P)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE156993 | GEO | 2020/08/28
REPOSITORIES: GEO
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Project description:Transcriptomic analysis of peripheral blood mononuclear cells (PBMC) of patients with type 2 Diabetes Melittus(T2DM), Dyslipidemia (DL) and Periodontitis (P)
| PRJNA659741 | ENA
Project description:Increased morbidity and mortality associated with post-ischemic heart failure (HF) in diabetic patients underscore the need for a better understanding of the underlying molecular events. Indeed, effective HF therapy in diabetic patients requires a complex strategy encompassing the development of improved diagnostic and prognostic markers and innovative pharmacological approaches. Whole mRNAs expression was measured in the heart of patients with heart failure (HF) with or without concomitant Type 2 diabetes mellitus (T2DM) and compared it to control non-failing hearts. We identified distinct genes modulated in HF patients compared to controls, as well as to T2DM HF patients compared to not diabetic HF patients. Our study included left ventricle (LV) cardiac biopsies taken from the vital, non-infarcted zone (remote zone) derived from patients affected by dilated hypokinetic post-ischemic cardiomyopathy, undergoing surgical ventricular restoration procedure. Inclusion criteria for diabetic were: GLICEMIA: >=126 mg/dl, previous T2DM diagnosis or anti-diabetic therapy, while for non diabetic: GLICEMIA: <100 mg/dl and HbA1c: n.v. 4.8-6.0%. Moreover, HF patients were matched for End Systolic Volume (ESV), Ejection fraction (LVEF), Age, Sex, Ethnic distribution, Smoke habits, Hypertension, Glomerular filtration rate (GFR), Body Mass Index (BMI). Genes expression was assessed by Affymetrix GeneChips Human Gene 1.0 ST array, using total RNA extracted from 7 T2DM HF patients, 12 non-T2DM HF patients and 5 controls.
2012-03-21 | E-GEOD-26887 | biostudies-arrayexpress
Project description:<p>Type 2 Diabetes Mellitus (T2DM) is a chronic and sometimes debilitating disease that affects millions of adults in the USA. Metformin is commonly prescribed for T2DM; yet some T2DM patients do not tolerate it or respond well. This pharmacogenomics study will examine response, as both change in T2DM patients' weight and hemoglobin A1c (HbA1c) levels, to different doses of metformin, by extracting this data from the electronic health record (EHR), for T2DM subjects taking metformin found by prescription orders in the EHR, and identified as cases with the EHR phenotype algorithm published by Kho et. al. in 2012 (PMID: <a href="http://www.ncbi.nlm.nih.gov/pubmed/22101970" target="_blank">22101970</a> as part of the eMERGE (electronic Medical Records and Genomics; dbGaP <a href="./study.cgi?study_id=phs000237">phs000237</a>, <a href="./study.cgi?study_id=phs000297">phs000297</a>, <a href="./study.cgi?study_id=phs000360">phs000360</a>, <a href="./study.cgi?study_id=phs000368">phs000368</a>, <a href="./study.cgi?study_id=phs000888">phs000888</a>, and <a href="./study.cgi?study_id=phs000948">phs000948</a>) project.</p>
| phs000984 | dbGaP
Project description:Skeletal muscle mitochondrial dysfunction is secondary to T2DM and can be improved by long-term regular exercise training Mitochondrial dysfunction has long been implicated to play a causative role in development of type 2 diabetes (T2DM). However, a growing number of recent studies provide data that mitochondrial dysfunction is a consequence of T2DM development. The aim of our study is to clarify in further detail the causal role of mitochondrial dysfunction in T2DM by a comprehensive ex vivo analysis of mitochondrial function combined with global gene expression analysis in muscle of pre-diabetic newly diagnosed untreated T2DM subjects and long-standing insulin treated T2DM subjects compared with age- and BMI-matched controls. In addition, we assessed the impact of long-term interval exercise training on physical activity performance, mitochondrial function and glycemic control in long-standing insulin-treated T2DM subjects. Ex vivo mitochondrial density, quality and functioning was comparable between pre-diabetic subjects and matched controls, however, gene expression analysis showed a switch from carbohydrate toward lipids as energy source in pre-diabetes subjects. In contrast, long-term insulin treated T2DM subjects had slightly decreased mitochondrial density and ex vivo function. Expression of Krebs cycle and OXPHOS related genes were decreased, indicating a decreased capacity to use lipids as an energy source. The insulin-treated T2DM subjects had a lower physical activity level than pre-diabetic and normoglycemic subjects. A 52 weeks exercise training of these subjects increased submaximal oxidative efficiency, increased in vivo PCr recovery rate, as well as mildly increased in vitro mitochondrial function. Gene expression of β-oxidation, Krebs cycle and OXPHOS-related genes was increased. Our data demonstrate that mitochondrial dysfunction is rather a consequence than a causative factor in T2DM development as it was only detected in overt diabetes and not in early diabetes. Regular exercise training stabilized exogenous insulin requirement and improved mitochondrial functioning, fatty acid oxidation and general physical work load capacity in long-standing insulin-treated T2DM subjects. As such, the present study shows for the first time that long-term exercise interventions are beneficial in this group of complex diabetes patient and may prevent further metabolic deterioration.
2010-11-29 | GSE19420 | GEO
Project description:Insulin resistance and Type 2 Diabetes Mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. To identify the underlying molecular processes in preadipocytes of T2DM patients that are a characteristic of the development of T2DM, preadipocyte cell cultures were prepared from subcutaneous fat biopsies of T2DM patients and compared with age- and BMI matched control subjects. Gene expression profiling showed changed expression of transcription factors involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were down-regulated, and inflammation/apoptosis was up-regulated in T2DM preadipocytes. The down-regulation of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage. 7 T2DM preadipocyte samples and 9 age- and BMI-matched control samples were hybridized using 70-mer oligonucleotide microarrays. Samples were labeled with either Cy3 or Cy5. A total of 20 arrays were used including dye swop. Per array, a T2DM sample was hybridized with a control sample of the same gender and matched based on age and BMI. To ensure hybridization of two samples with the same gender, three T2DM (5064, 5128, 5395) and one control sample (5616) were used twice and listed as technical replicates.
2010-05-16 | E-GEOD-15790 | biostudies-arrayexpress
Project description:Objective: To explore the mechanism of Jiangtang Tiaozhi Recipe in the treatment of obese T2DM patients with dyslipidemia based on transcriptomics. Methods: We chose 6 patients with obese type 2 diabetes mellitus and dyslipidemia (syndrome of excess of gastrointestinal heat) who were treated by JTTZR for 24 weeks, while 6 cases included in the healthy control group. We selected 6 cases in each group (disease group before treatment, disease group after treatment and healthy control group) to start the research of lncRNA microarray. According to the differentially expressions of lncRNAs and mRNAs, we secondly performed GO analysis, Pathway analysis, and found out some target lncRNAs as well as their associated mRNAs. The trial register number is NCT04623567. Results: (1) Disease group before treatment vs. healthy control group: There are 557 upregulated lncRNAs, 273 downregulated lncRNAs, 491 upregulated mRNAs and 1639 downregulated mRNAs. (2) Disease group after treatment vs. Disease group before treatment: There are 128 upregulated lncRNAs, 32 downregulated lncRNAs, 45 upregulated mRNAs and 140 downregulated mRNAs.
2022-01-14 | GSE193626 | GEO
Project description:Insulin resistance and Type 2 Diabetes Mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. To identify the underlying molecular processes in preadipocytes of T2DM patients that are a characteristic of the development of T2DM, preadipocyte cell cultures were prepared from subcutaneous fat biopsies of T2DM patients and compared with age- and BMI matched control subjects. Gene expression profiling showed changed expression of transcription factors involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were down-regulated, and inflammation/apoptosis was up-regulated in T2DM preadipocytes. The down-regulation of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage.
2009-12-31 | GSE15790 | GEO
Project description:Here, we performed a genome-wide promoter analysis of DNA methylation to screen for genes differentially methylated in T2DM.<br>We used methylated DNA immunoprecipitation (MeDIP), combined with microarray technology (Keshet et al., 2006; Weber et al., 2005), to discover whether changes in DNA methylation are specific to T2DM. A cohort of normal glucose tolerant (NGT) and Type 2 diabetic (T2DM) male volunteers was studied.
2010-07-15 | E-MEXP-2253 | biostudies-arrayexpress
Project description:Pseudoalteromonas sp. DL-6 Genome sequencing
| PRJNA374396 | ENA
Project description:Pseudoalteromonas sp. DL-6 Genome sequencing
| PRJNA373964 | ENA