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Transcriptomics analysis of skeletal muscle in type 2 diabetes patients

ABSTRACT: Transcriptomics analysis of skeletal muscle in type 2 diabetes patients

PROVIDER: PRJEB37684 | ENA |

REPOSITORIES: ENA

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			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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Transcriptomics analysis of skeletal muscle in type 2 diabetes patients

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:The current study aimed to address the hypothesis that programmed expression of key miRNAs in skeletal muscle mediates the development of insulin resistance, and consequently long-term health. We thus examined microRNA signatures in skeletal muscle of unmedicated newly diagnosed human pre-diabetics and type 2 diabetics. Skeletal muscle biopsies were obtained from the vastus lateralis from males with pre-diabetes (PD, n=5) or type 2 diabetes mellitus (T2DM, n=6) along with age and sex-matched healthy volunteers (H, n=5). Ramaciotti Centre for Genomics (UNSW, sydney, Australia)

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Human skeletal muscle CD90+ fibro-adipogenic progenitors are associated with muscle degeneration in type 2 diabetic patients

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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Distinctive exercise-induced inflammatory response and exerkine induction in skeletal muscle of people with type 2 diabetes

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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Dysregulated Skeletal Muscle Myosin Super-relaxation in Type II, but Not Type I, Diabetes Mellitus

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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Downregulation of Human-Specific lncRNA TMEM9B-AS1 in Skeletal Muscle of People with Type 2 Diabetes Impacts Ribosomal Biogenesis

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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