Project description:Type 2 diabetes is one of the most prevalent metabolic disorders. It is characterised by insulin resistance in peripheral tissues. Skeletal muscle is one of the tissues that affect by insulin resistance. Therefore, the study aims to identify differentially regulated genes in skeletal muscle of type 2 diabetes patients. Here, we obtained biopsies from the pectoralis major muscle and performed RNA sequencing to profile the gene expression patterns from four patients with diabetes and three healthy controls.
Project description:Patients with hypertension alone, hypertension plus controlled diabetes and hypertension plus uncontrolled diabetes, and control patients without these conditions underwent coronary artery bypass grafting surgery. Skeletal muscle biopsy specimens were taken at the beginning ('pre-operative') and at the end ('post-operative') of the surgery.
Project description:Global transcript profiling to identify differentially expressed skeletal muscle genes in insulin resistance, a major risk factor for Type II (non-insulin-dependent) diabetes mellitus. Compared gene expression profiles of skeletal muscle tissues from 18 insulin-sensitive versus 17 insulin-resistant equally obese, non-diabetic Pima Indians. Keywords: other
Project description:Aging and type 2 diabetes mellitus (T2DM) are associated with impaired skeletal muscle function and degeneration of the skeletal muscle microenvironment. However, the origin and mechanisms underlying the degeneration are not well described in human skeletal muscle. Here we show that skeletal muscles of T2DM patients exhibit pathological degenerative remodeling of the extracellular matrix that was associated with a selective increase of a subpopulation of fibro-adipogenic progenitors (FAPs) marked by expression of THY1 (CD90).
Project description:Myotonic Dystrophy Type-2 (DM2) is an autosomal dominant disease caused by the expansion of a CCTG tetraplet repeat. It is a multisystemic disorder, affecting skeletal muscles, the heart, the eye, the central nervous system and the endocrine system. Whole mRNAs expression was measured in the muscle of DM2 patients and compared it to controls.We identified distinct genes modulated in DM2 patients compared to controls. Our study included 10 DM2 and 10 control (CTR) muscle biopsies from biceps brachii. DM2 and CTR were age- and sex- matched. Most DM2 patients had myotonia and cataract, two disease hallmarks, while differences in other clinical parameters (muscle strenght, diabetes, CPK, FT3, FT4, TSH, ejection fraction) were not significant. Genes expression was assessed by Affymetrix Gene Chip Human Exon 1.0 ST Array.
Project description:Myotonic Dystrophy Type-2 (DM2) is an autosomal dominant disease caused by the expansion of a CCTG tetraplet repeat. It is a multisystemic disorder, affecting skeletal muscles, the heart, the eye, the central nervous system and the endocrine system The expression of 365 miRNAs was measured in the muscle of DM2 patients and compared it to controls and were identified distinct miRNAs modulated in DM2 patients compared to controls. Our study included 10 DM2 and 9 control (CTR) muscle biopsies from biceps brachii. DM2 and CTR were age- and sex- matched. Most DM2 patients had myotonia and cataract, two disease hallmarks, while differences in other clinical parameters (muscle strenght, diabetes, CPK, FT3, FT4, TSH, ejection fraction) were not significant. miRNAs expression was assessed by Applied Biosystems Human TaqMan Low Density Array (TLDA, v1.0).
Project description:We performed gene expression microarray analysis of skeletal muscle biopsies from normal glucose tolerant subjects and type 2 diabetes subjects obtained during a 60 min bicycle ergometer exercise and the 180 min of recovery phase We analysed skeletal mucle biopsies from patients with T2D and from control subjects (n=7 each) at three time points during exercise and recovery
Project description:The targeted muscle insulin receptor knockout (MIRKO) model was used, in which there is a complete absence of the insulin-receptor signaling in skeletal muscle but normal insulin and glucose levels. By comparing skeletal muscle gene-expression profiles from MIRKO mice and their controls (lox/lox) under three different metabolic conditions (namely, in the basal state, after streptozotocin (STZ)-induced diabetes, and after STZ-induced diabetes rendered euglycemic with insulin treatment), we can address the following three important questions. (i) What is the direct effect of the loss of insulin signaling on gene expression in skeletal muscle? (ii) What is the contribution of the metabolic and other changes that accompany diabetes to induce indirect changes in gene expression? (iii) How are these pathways regulated and implicated in the pathophysiology of diabetes?
Project description:The nucleosome signature reflects the cellular epigenetic memory and contributes to the cellular phenotype and function. Obesity and type 2 diabetes pathogenesis is largely dependent on environmentally-induced epigenetic modifications and is marked by skeletal muscle insulin resistance; however, no in vivo skeletal muscle nucleosome maps exist to date. Herein, whole genome nucleosome maps via MNase-seq in skeletal muscle of mice on a low fat, high fat or high fat diet with the chromatin modifier sodium butyrate show that complex interactions among mitochondrial function, the tissue microenvironment, cellular phenotype and nucleosome landscape determine whole body phenotype and insulin resistance. Skeletal muscle samples (n=5 per group) were pooled after homogenization under liquid nitrogen with a motar and pestle to give one sample per group for MNase-seq
Project description:Microarray-based studies of skeletal muscle from patients with type 2 diabetes and high-risk individuals have demonstrated that insulin resistance and reduced mitochondrial biogenesis co-exist early in the pathogenesis of type 2 diabetes independent of hyperglycaemia and obesity. It is unknown whether reduced mitochondrial biogenesis or other transcriptional alterations co-exist with impaired insulin-responsiveness in primary human muscle cells from patients with type 2 diabetes. Results: No single gene was differently expressed after correction for multiple testing, and no biological pathway was differently expressed using both approaches for global pathway analysis. In particular, we found no evidence for differential expression of genes involved in mitochondrial oxidative metabolism. Consistently, there was no difference in mRNA levels of genes known to mediate the transcriptional control of mitochondrial biogenesis, PPARGC1A and NRF-1, or in mitochondrial mass between diabetic and control myotubes. Keywords: Cell culture, genetic, oxidative phosphorylation, microarray, skeletal muscle, type 2 diabetes