Transcriptomic profiles of skeletal muscle tissue following an euglycemic-hyperinsulinemic clamp in insulin-resistant obese subjects

Rudkowska, Iwona; Jacques, Hélène; Weisnagel, S. John; Marette, André; Vohl, Marie‐Claude

doi:10.1007/s12263-012-0298-2

Cited by 7 publications

(4 citation statements)

References 33 publications

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“…At 90 min, 62% (275 out of 442) genes were upregulated and 38% (167 out of 442) were downregulated in response to insulin, and similar percentages of upregulated and downregulated genes were seen after 6 hours of insulin. The higher proportion of genes that is upregulated is consistent with the anabolic role of insulin, and a microarray study of gene expression changes in skeletal muscle after a 3-hour hyperinsulenemic clamp 63 . The insulin-induced gene expression changes in our study suggest regulation of various KEGG-based pathways, including Rap1, Ras, PI3K-Akt and MAPK signaling as well as ABC transporter function, consistent with a hepatoma and liver RNA-Seq study 6,64 and other insulin studies 3,65–67 .…”

Section: Discussionmentioning

confidence: 56%

Integration of TGF-β-induced Smad signaling in the insulin-induced transcriptional response in endothelial cells

Budi

Hoffman

Gao

et al. 2019

Sci Rep

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Insulin signaling governs many processes including glucose homeostasis and metabolism, and is therapeutically used to treat hyperglycemia in diabetes. We demonstrated that insulin-induced Akt activation enhances the sensitivity to TGF-β by directing an increase in cell surface TGF-β receptors from a pool of intracellular TGF-β receptors. Consequently, increased autocrine TGF-β signaling in response to insulin participates in insulin-induced angiogenic responses of endothelial cells. With TGF-β signaling controlling many cell responses, including differentiation and extracellular matrix deposition, and pathologically promoting fibrosis and cancer cell dissemination, we addressed to which extent autocrine TGF-β signaling participates in insulin-induced gene responses of human endothelial cells. Transcriptome analyses of the insulin response, in the absence or presence of a TGF-β receptor kinase inhibitor, revealed substantial positive and negative contributions of autocrine TGF-β signaling in insulin-responsive gene responses. Furthermore, insulin-induced responses of many genes depended on or resulted from autocrine TGF-β signaling. Our analyses also highlight extensive contributions of autocrine TGF-β signaling to basal gene expression in the absence of insulin, and identified many novel TGF-β-responsive genes. This data resource may aid in the appreciation of the roles of autocrine TGF-β signaling in normal physiological responses to insulin, and implications of therapeutic insulin usage.

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Section: Discussionmentioning

confidence: 56%

Integration of TGF-β-induced Smad signaling in the insulin-induced transcriptional response in endothelial cells

Budi

Hoffman

Gao

et al. 2019

Sci Rep

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“…For example, skeletal muscle was profiled in obese subjects with insulin resistance (n=15) at 4 time points after supplementation with n-3 PUFA or n-3 PUFA with fish gelatin, in both cases before and after a euglycemic-hyperinsulinemic clamp. 107 This approach allowed identification of genes that were robustly altered by the clamp and by supplementation itself. This group has also used response to intervention as a tool to understand genetic differences in transcriptomic responses.…”

Section: Unbiased Transcriptomicsmentioning

confidence: 99%

Nutrigenomics, the Microbiome, and Gene-Environment Interactions: New Directions in Cardiovascular Disease Research, Prevention, and Treatment

Ferguson¹,

Allayee²,

Gerszten³

et al. 2016

Circ Cardiovasc Genet

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Abstract-Cardiometabolic diseases are the leading cause of death worldwide and are strongly linked to both genetic and nutritional factors. The field of nutrigenomics encompasses multiple approaches aimed at understanding the effects of diet on health or disease development, including nutrigenetic studies investigating the relationship between genetic variants and diet in modulating cardiometabolic risk, as well as the effects of dietary components on multiple "omic" measures, including transcriptomics, metabolomics, proteomics, lipidomics, epigenetic modifications, and the microbiome. Here, we describe the current state of the field of nutrigenomics with respect to cardiometabolic disease research and outline a direction for the integration of multiple omics techniques in future nutrigenomic studies aimed at understanding mechanisms and developing new therapeutic options for cardiometabolic disease treatment and prevention. The interpretation and scope of nutrigenomics may vary, but it can be thought to encompass the spectrum of nutritional genomics research, including classic nutrigenetics studies of gene-diet interactions and molecular nutrition, in vitro and in vivo models, human nutrition studies, and the application of largescale, unbiased studies using high-throughput "omics" techniques to study the effects of nutrients on the body. 6 As the Figure shows, diet and the genome may influence cardiometabolic health through a variety of interconnected intermediates, perturbations in which can be measured through omics technologies, including RNA expression (transcriptome), epigenetic modifications (epigenome), metabolites (metabolome), lipids (lipidome), proteins (proteome), and resident microbial communities (microbiome). Although it is clear that both nutrients and genes play a distinct role in determining health, the complex interactions among genes, diet, and downstream networks are not well understood. The application of nutrigenomics approaches to questions of human health and disease is an important component in understanding the complexities of the interplay between basic metabolic processes and externalThe American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on January 22, 2016, and the American Heart Association Executive Committee on February 23, 2016. A copy of the document is available at http://professional.heart.org/statements by using either "Search for Guidelines & Statements" or the "Browse by Topic" area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@ wolterskluwer.com.The...

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“…Metabolic pathways that incorporated, inflammatory signaling and nuclear receptors were also significantly different. These included LXR/RXR activation, VDR/RXR activation, interleukin IL-8, acute phase response, IL-10, triggering receptor expressed on myeloid cells 1, peroxisome proliferator-activated receptor, G-beta/gamma and hepatocyte growth factor and IL6 signaling (Rudkowska et al, 2013 ).…”

Section: The Role Of Vitamin D Receptor In Muscle Functionmentioning

confidence: 99%

The role of vitamin D in skeletal and cardiac muscle function

Polly

Tan

2014

Front. Physiol.

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Myopathy is a feature of many inflammatory syndromes. Chronic inflammation has been linked to pathophysiological mechanisms which implicate 1,25 dihydroxyvitamin D3 (1,25-(OH)2D3)-mediated signaling pathways with emerging evidence supporting a role for the vitamin D receptor (VDR) in contractile and metabolic function of both skeletal and cardiac muscle. Altered VDR expression in skeletal and cardiac muscle has been reported to result in significant effects on metabolism, calcium signaling and fibrosis in these tissues. Elevated levels of serum inflammatory cytokines, such as IL-6, TNF-α and IFNγ, have been shown to impact myogenic and nuclear receptor signaling pathways in cancer-induced cachexia. The dysregulation of nuclear receptors, such as VDR and RXRα in muscle cells, has also been postulated to result in myopathy via their effects on muscle structural integrity and metabolism. Future research directions include generating transcriptome-wide information incorporating VDR and its gene targets and using systems biology approaches to identify altered molecular networks in human tissues such as muscle. These approaches will aid in the development of novel therapeutic targeting strategies for inflammation-induced myopathies.

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Transcriptomic profiles of skeletal muscle tissue following an euglycemic-hyperinsulinemic clamp in insulin-resistant obese subjects

Cited by 7 publications

References 33 publications

Integration of TGF-β-induced Smad signaling in the insulin-induced transcriptional response in endothelial cells

Integration of TGF-β-induced Smad signaling in the insulin-induced transcriptional response in endothelial cells

Nutrigenomics, the Microbiome, and Gene-Environment Interactions: New Directions in Cardiovascular Disease Research, Prevention, and Treatment

The role of vitamin D in skeletal and cardiac muscle function

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