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MicroRNA signature in skeletal muscle in type 2 Diabetes [human]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE68224 | GEO | 2015/04/25

SECONDARY ACCESSION(S): PRJNA282055

REPOSITORIES: GEO

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MicroRNA signature in skeletal muscle in type 2 Diabetes [human]

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)

2015-04-25 | E-GEOD-68224 | biostudies-arrayexpress

MicroRNA signature in skeletal muscle in insulin resistant rats

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 programmed insulin resistant rats offspring from high fat-fed dams vs control offspring from chow fed dams. Skeletal muscle (soleus) was collected from the hind limb of 1 year old male offspring (6 from control dams, 6 from high fat-fed dams) . Ramaciotti Centre for Genomics (UNSW, sydney, Australia)

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MicroRNA signature in skeletal muscle in insulin resistant rats

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Muscle - atypical diabetes protein expression

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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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ZAKb is a cellular compression sensor that mediates hypertrophic signaling in skeletal muscle

Project description:Mechanosensing is required for the senses of touch and hearing, and impacts on cellular processes such as cell differentiation, migration, invasion and tissue homeostasis. Mechanical inputs give rise to p38- and JNK-signaling, which mediates adaptive physiological responses in various tissues. In muscle, fiber contraction-induced p38 and JNK signaling ensures adaptation to exercise, muscle repair and hypertrophy. However, the mechanism by which muscle fibers sense mechanical load to activate this signaling, as well as the physiological roles of mechanical stress sensing more broadly, have remained elusive. Here, we show that the upstream MAP3K ZAK is a sensor of cellular compression induced by osmotic shock and cyclic compression in vitro, and muscle contraction in vivo. This function relies on ZAK’s ability to recognize stress fibers in cells and the corresponding Z-discs in muscle fibers, when under tension. Consequently, ZAK-deficient mice present with skeletal muscle defects characterized by fibers with centralized nuclei and progressive adaptation towards a slower myosin profile. Our results highlight how cells in general sense mechanical compressive load, and how mechanical forces generated during muscle contraction are translated into MAP kinase signaling.

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Project description:In differentiated skeletal muscle, intracellular Ca2+ concentrations rise dramatically upon membrane depolarization, constituting the link between excitation and contraction (EC). Transient rises in [Ca2+]i mainly emerge from Ca2+ released by the type 1 ryanodine receptor (RYR1) and, in non-adult muscle, by the inositol 1,4,5-triphosphate receptor (IP3R) of the sarcoplasmic reticulum (SR), the dominant Ca2+ store in skeletal muscle. While the IP3R-mediated, slow Ca2+ transients, have been implicated in cell signaling and development, RYR1’s non-contractile role(s) remain obscure. We used a homozygous mouse RyR1 knockout model (dyspedic) to investigate the effects of the absence of a functional RYR1 and, consequently, the lack of RyR1-mediated Ca2+ signaling during embryogenesis. While heterozygous mice of the model are undistinguishable from WT littermates, homozygous dyspedic mice die at birth from asphyxia, since their skeletal muscle does not support EC coupling. Furthermore, they display abnormal spine curvature, subcutaneous hematomas, small limbs, and enlarged neck. Skeletal muscles from front and hind limbs of dyspedic embryos (day E18.5) were subjected to microarray analyses, revealing 318 genes, significantly regulated by at least 50 % compared to control heterozygous littermates.

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