Effect of long-term exercise training on lncRNAs expression in the vascular injury of insulin resistance
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ABSTRACT:
PROVIDER: PRJNA480602 | ENA |
REPOSITORIES: ENA
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Project description:The present study identified a panel of dysregulated lncRNAs and mRNAs that might serve as potential biomarkers relevant to the vascular injury in insulin resistance induced by high-fat diet. Exercise might alleviate the vascular injury in insulin resistance via targeting FR402720 and FR030200.
2019-12-31 | GSE116917 | GEO
Project description:We reported that skeletal muscle insulin sensitivity was restored to a lean phenotype with exercise training in patients undergoing RYGB surgery. For that, the goals of this study is to identify changes in the skeletal muscle transcriptome profiling (RNA-seq) that could explain the insulin sensitivity improvement of RYGB + exercise training group.
2020-05-19 | GSE137631 | GEO
Project description:Experiment designed to identify differences in gene expression patterns in previously sedentary individuals before an endurance exercise training program. This series compares 2 groups of individuals that display high and low insulin sensitivity (SI) response (HSIR and LSIR) after 20 weeks of exercise (a 4-fold difference in SI response). There were no differences before training for SI, sex, age, BMI or body fat in the individuals integrating the LSIR and HSIR groups. Keywords = skeletal muscle Keywords = exercise-training Keywords = insulin sensitivity Keywords: repeat sample
2005-02-14 | GSE1718 | GEO
Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFβ signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease.
2014-05-23 | GSE57880 | GEO
Project description:Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are exercise resistant, and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise resistant phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFM-NM-2 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Cardiac and skeletal muscle from 3 high and 3 low responder rats were examined for differential miRNA expression using Exiqon microarrays
2014-05-23 | E-GEOD-57880 | biostudies-arrayexpress
Project description:The overall objective of the heritage project is to study the role of the genotype in cardiovascular,metabolic and hormonal responses to aerobic exercise training and the contribution of regular exercise to changes in several cardiovascular disease and diabetes risk factors. PLEASE NOTE THE POST-TRAINING GENE CHIP FILES HAVE NEVER BEEN RELEASED ON GEO. PLEASE ALSO NOTE THAT DUE TO THE OUTDATED INSULIN ASSAY UTILISED IN THE HERITAGE STUDY, THE INSULIN DATA WAS NOT COMPARABLE WITH ANY MORE RECENT MODERN STUDIES.
2013-06-12 | GSE47874 | GEO
Project description:We assessed vastus lateralis muscle gene expression levels of 12 women with the metabolic syndrome before and after a 6 month exercise training program RNA was isolated from a vastus lateralis muscle biopsy of 6 women with the metabolic syndrome before and after a 6 month guided endurance exercise training program
2013-11-05 | E-GEOD-43760 | biostudies-arrayexpress
Project description:This study aimed to determine skeletal muscle DNA methylation changes in a cohort of volunteers with a range of insulin sensitivities following 8-weeks of supervised exercise training. We studied 13 sedentary participants (5M/8F, 34.6 ± 3.1 years) and performed euglycemic hyperinsulinemic clamps with vastus lateralis muscle biopsies and peak aerobic activity (VO2 peak) tests before and after training. We extracted DNA from the muscle biopsies and performed global methylation using Illumina's Methylation EPIC 850K BeadChip.
2022-03-01 | E-MTAB-11282 | biostudies-arrayexpress
Project description:Endurance exercise training has been shown to decrease whole-body and skeletal muscle insulin resistance and increase glucose tolerance in conditions of both pre-diabetes and overt type 2 diabetes. However, the adaptive responses in skeletal muscle at the molecular and genetic level for these beneficial effects of exercise training have not been clearly established in an animal model of pre-diabetes. The present study identifies alterations in skeletal muscle gene expression that occur with exercise training in pre-diabetic, insulin-resistant obese Zucker (fa/fa) rats and insulin-sensitive lean Zucker (Fa/-) rats. Treadmill running for up to 4 weeks caused significant enhancements of glucose tolerance as assessed by the integrated area under the curve for glucose (AUCg) during an oral glucose tolerance test in both lean and obese animals. Using microarray analysis, a set of only 12 genes was identified as both significantly altered (>1.5-fold change relative to sedentary controls; p<0.05) and significantly correlated (p<0.05) with the AUCg. Two of these genes, peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a) and the z-isoform of protein kinase C (PKC-z), have known involvement in the regulation of skeletal muscle glucose transport. We confirmed that protein expression levels of PGC-1a and PKC-z were positively correlated with the mRNA expression levels for these two genes. Overall, this study has identified a limited number of genes in soleus muscle of lean and obese Zucker rats that are associated with decreased insulin resistance and increase glucose tolerance following endurance exercise training. These findings could guide the development of pharmaceutical M-^Sexercise mimeticsM-^T in the treatment of insulin-resistant, pre-diabetic or overtly type 2 diabetic individuals.
2009-11-16 | E-TABM-213 | biostudies-arrayexpress
Project description:oat bran & exercise training Raw sequence reads
| PRJNA1167239 | ENA