Transcriptomics analysis of skeletal muscle in type 2 diabetes patients
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB37684 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4010590.fastq.gz | Fastqsanger.gz | |||
| ERR4010591.fastq.gz | Fastqsanger.gz | |||
| ERR4010592.fastq.gz | Fastqsanger.gz | |||
| ERR4010593.fastq.gz | Fastqsanger.gz | |||
| ERR4010594.fastq.gz | Fastqsanger.gz |
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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.
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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).
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Project description:Mechanistic insights into the molecular events by which exercise enhances the skeletal muscle phenotype are lacking, particularly in the context of type 2 diabetes. Here we unravel a fundamental role for exercise-responsive cytokines (exerkines) on skeletal muscle development and growth in individuals with normal glucose tolerance or type 2 diabetes. Acute exercise triggered an inflammatory response in skeletal muscle, concomitant with an infiltration of immune cells. These exercise effects were potentiated in type 2 diabetes. In response to contraction or hypoxia, cytokines were mainly produced by endothelial cells and macrophages. The chemokine CXCL12 was induced by hypoxia in endothelial cells, as well as by conditioned medium from contracted myotubes in macrophages. We found that CXCL12 was associated with skeletal muscle remodeling after exercise and differentiation of cultured muscle. Collectively, acute aerobic exercise mounts a non-canonical inflammatory response, with an atypical production of exerkines, which is potentiated in type 2 diabetes.
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Project description:Skeletal muscle plays a critical role in the onset and development of type II diabetes. However, very few studies have investigated the potential pathogenic role of its most abundant protein, myosin. Hence, here, we aim to define this by focusing on myosin energy-saving state known as super-relaxed state (SRX). We performed an array of (loaded Mant-ATP chase experiments, LC-MS/MS proteomics, X-ray diffraction) assays on vastus lateralis biopsies from diabetic patients and matched controls. Strikingly, our results highlight that the amount of muscle myosin molecules in SRX is higher and the related ATP demand lower in type II diabetes patients than in controls. These physiological changes are parallel with greater glycation levels on myosin heavy chains, and with remodeled sarcomeric proteins in the same type II diabetes patients. None of these (mal)adaptations were noticed in patients with type I diabetes. Altogether, our findings emphasize a complex molecular dysregulation of myosin SRX and ATP consumption in type II diabetes. Ultimately, pharmacological targeting of SRX could benefit whole-body metabolic health through the enhancement of energy expenditure.
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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).
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Project description:The emergence and progression of type 2 diabetes mellitus (T2DM) are intricately linked to skeletal muscle loss, yet the exact mechanisms remain elusive. Here, our whole-exome and transcriptomic results indicate that VAV3 is mutated and down-regulated in T2DM patients associated with increased sulfur metabolism. Integrated analysis of human transcriptomics, mouse and cellular proteomics, glycol-metabolomics analyses suggest a potential association between VAV3, T2DM and disulfidptosis. Inhibiting disulfidptosis or SLC7A11/3A2 rescues death of Vav3-deleted cells and IR cells. Mechanistically, Vav3 deletion leads to decreased mitochondrial ATP synthesis and reduced GLUT4 expression. Insufficient glucose intake combined with elevated SLC7A11/3A2 expression induces NADPH depletion and cystine accumulation, leading to redox system imbalance and aberrant disulfide bonds formation. This results in F-actin collapse, broken fiber bundles and rapid cell death. Together, our findings reveal unexpected roles of VAV3 in regulating glucose metabolism, disulfidptosis and provide a therapeutic strategy to target skeletal muscle disulfdptosis in T2DM treatment.
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Project description:Long non-coding RNAs (lncRNAs) are important regulators of skeletal muscle physiology, with altered expression noted in several human diseases including type 2 diabetes. Here we report downregulation of TMEM9B-AS1, a previously uncharacterized lncRNA, in skeletal muscle of men with type 2 diabetes. We demonstrate that loss of TMEM9B-AS1 in primary human myotubes leads to reduction in protein synthesis, concomitant with reduced phosphorylation of ribosomal protein S6, downstream of ERK and mTOR pathways. Moreover, we show that TMEM9B-AS1 plays a pivotal role in the regulation of ribosomal biogenesis by facilitating mRNA stabilization of the transcription factor MYC through a direct physical interaction with the RNA-binding protein IGF2BP1. Disrupted ribosomal biogenesis resulting from downregulation of TMEM9B-AS1 links to the decrease in skeletal muscle mass observed in individuals with type 2 diabetes, shedding new light on the molecular mechanisms underlying this metabolic disorder.
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