Rattus norvegicus
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PROVIDER: PRJNA140401 | ENA |
REPOSITORIES: ENA
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Project description:Background: Insulin's effect on protein synthesis (translation of transcripts) and post-translational modifications, especially those involving reversible modifications such as phosphorylation of various signaling proteins, are extensively studied. On the other hand, insulin's effect on the transcription of genes, especially of transcriptional temporal patterns, is not well investigated in the literature. Methods: To identify significant transcriptional temporal patterns, primary differentiated rat skeletal muscle myotubes were treated with insulin and samples were collected every 10 min for 8 hours. Pooled samples at every hour were analyzed by a gene array approach to measure transcript levels. The pattern of transcript levels were analyzed based on a novel method that integrates selection, clustering, and functional annotation to find the main temporal patterns associated with functional groups of differentially expressed genes. Conclusion: In response to insulin, 326 genes were selected as differentially expressed in response to in vitro insulin treatment in skeletal muscle myotubes. Approximately 20% of the genes that were differentially expressed were identified as belonging to the insulin signaling pathway. 12 different clusters of gene expression profiles are identified which shows patterns that includes a slow and gradual decrease in gene expression, a gradual increase in gene expression reaching a peak at about 5 hours and then reaching a plateau or an initial decrease and other different variable patterns of increase in gene expression over time. As far as we know, this is the first systematic study in the literature monitoring transcriptional response to insulin in endothelial cells, in a time series microarray experiment.
2012-05-03 | GSE28997 | GEO
Project description:Background: Insulin's effect on protein synthesis (translation of transcripts) and post-translational modifications, especially those involving reversible modifications such as phosphorylation of various signaling proteins, are extensively studied. On the other hand, insulin's effect on the transcription of genes, especially of transcriptional temporal patterns, is not well investigated in the literature. Methods: To identify significant transcriptional temporal patterns, primary differentiated rat skeletal muscle myotubes were treated with insulin and samples were collected every 10 min for 8 hours. Pooled samples at every hour were analyzed by a gene array approach to measure transcript levels. The pattern of transcript levels were analyzed based on a novel method that integrates selection, clustering, and functional annotation to find the main temporal patterns associated with functional groups of differentially expressed genes. Conclusion: In response to insulin, 326 genes were selected as differentially expressed in response to in vitro insulin treatment in skeletal muscle myotubes. Approximately 20% of the genes that were differentially expressed were identified as belonging to the insulin signaling pathway. 12 different clusters of gene expression profiles are identified which shows patterns that includes a slow and gradual decrease in gene expression, a gradual increase in gene expression reaching a peak at about 5 hours and then reaching a plateau or an initial decrease and other different variable patterns of increase in gene expression over time. As far as we know, this is the first systematic study in the literature monitoring transcriptional response to insulin in endothelial cells, in a time series microarray experiment. The purpose of this investigation was to examine the transcriptional response of skeletal muscle cells during acute insulin stimulation. Samples were collected at times 0, 20, 40, 60, . . . , 480 minutes (every 20 minutes, for 8 hours) from both insulin treated and control cultures, for a total of 50 biological samples. Samples (20, 40, 60), (80, 100, 120), (140, 160, 180), (200, 220, 240), (260, 280, 300), (320, 340, 360), (380, 400, 420) and (440, 460, 480) from insulin-treated and control cultures were pooled together, obtaining eight joint samples. Consistently, sample 0’ was harvested and collected in triplicates and pooled together (0a, 0b, 0c) for each culture and two targets for the hybridization were prepared separately. All of the culturing and sampling procedures described above were repeated two additional times on different days, using the same identical cell line, to obtain a complete triplicate of the experiment. Sample 'Insulin_3_rep_a' (pool of 140', 160', 180') was excluded from the analysis since it had quite poor MvA plots compared to the median microarray signal.
2012-05-02 | E-GEOD-28997 | biostudies-arrayexpress
Project description:Aging laryngeal muscle: shifts in gene expression patterns and function
| PRJNA92829 | ENA
Project description:Insulin-stimulated muscle glucose uptake is a key process to alleviate hyperglycemia. This process depends on the redistribution of glucose transporters to the muscle surface membrane following phosphorylation of TBC1D1 and TBC1D4. Genetic evidence from a TBC1D4 loss-of-function mutation in human skeletal muscle is associated with an increased risk of type 2 diabetes (T2D). However, little is known about the potential regulating interactors of TBC1D4 in skeletal muscle. Here, we sought to identify interactors of TBC1D4 in human skeletal muscle by an unbiased proteomics approach. We detected 76 proteins as candidate TBC1D4 interactors, whereof 12 were regulated by insulin stimulation including known proteins involved in glucose metabolism (e.g. 14-3-3 proteins and ACTN4). TBC1D1 also co-precipitated with TBC1D4 and vice versa in both human and mouse skeletal muscle. This interaction was not regulated by insulin or exercise in young healthy lean individuals. In contrast, we observed an altered interaction as well as compromised insulin-stimulated phospho-regulation of the TBC1D1-TBC1D4 complex in muscle of obese individuals with T2D. In conclusion, we provide a list of TBC1D4 interactors in human and mouse skeletal muscle. These protein interactors serve as potential regulators of TBC1D4 function and thus insulin-stimulated glucose uptake in skeletal muscle.
2022-03-01 | PXD026225 | Pride
Project description:The aim of this project is to identify distinct temporal patterns of RNA expression in the skeletal muscle of rats following a bolus dose of the corticosteroid methylprednisolone. 51 RG_U34A chips were used over 17 time points.
2007-10-10 | E-GEOD-490 | biostudies-arrayexpress
Project description:Identifying Significant Temporal Variation in Time Course Microarray Data Without Replicates
| PRJNA113577 | ENA
Project description:Using mass spectrometry-based phosphoproteomics, we quantified 23,126 phosphosites in the skeletal muscle of five genetically distinct inbred mouse strains exposed to two controlled dietary environments, with and without acute insulin treatment. Almost half of the insulin-regulated phosphoproteome was altered by genetic background independently of diet, and high-fat high-sugar feeding also affected insulin signalling in a strain-dependent manner. Our data illuminated signalling network organisation principles, including the uncoupling of phosphosites targeted by the same kinase. Associating diverse signalling responses with insulin-stimulated glucose uptake uncovered regulators of muscle insulin responsiveness, including the regulatory phosphosite S469 on Pfkfb2, a key glycolytic enzyme.
2023-12-21 | PXD041229 | Pride
Project description:Studies in rodents have shown obesity and aging impair tissue nicotinamide adenine dinucleotide (NAD+) biosynthesis, which contributes to metabolic dysfunction. The availability of nicotinamide mononucleotide (NMN) is an important rate-limiting factor in mammalian NAD+ biosynthesis. We conducted a 10-week, randomized, placebo-controlled, double-blind trial to evaluate the effect of NMN supplementation on metabolic function in 25 postmenopausal women with prediabetes who were overweight/obese. Insulin-stimulated glucose disposal, assessed by using the hyperinsulinemic-euglycemic-clamp procedure, increased by 25±7% (P<0.01) in the NMN group, which was accompanied by an increase in insulin-stimulated phosphorylation of muscle AKT (P<0.01), whereas neither outcome changed after placebo treatment. Body composition (fat mass, fat-free mass, intra-abdominal fat, intrahepatic triglyceride content) and muscle mitochondrial respiratory capacity did not change after treatment with placebo or NMN. These results demonstrate NMN improves muscle insulin sensitivity in women with prediabetes who are overweight/obese, independent of changes in body composition or mitochondrial function.
2021-05-01 | GSE157988 | GEO
Project description:Lifestyle intervention including exercise restores glucose homeostasis and pancreatic β-cell function in type 2 diabetes (T2D). However, exercise compliance is a challenge. Novel alternative or adjuvant approaches are necessary. During exercise, the contracting skeletal muscle acts as endocrine organ via the secretion and endocrine signaling of functional proteins. We postulated that contracting skeletal muscle secretes proteins that target pancreatic β-cells and regulate insulin secretion and glucose metabolism. To test this hypothesis, we used an in vitro cell-based skeletal muscle contraction system to uncover proteins released in the muscle secretome. Using an RNAseq screen, we identified growth differentiation factor 15 (GDF15) as a lead candidate. β-cells, human pancreatic islets, and C57BL/6J mice exposed to acute GDF15 treatment exhibited increased glucose-stimulated insulin secretion, and the mechanism involved activation of the insulin release pathway. Chronic GDF15 treatment in db/db mice reduced insulin resistance and preserved pancreatic PDX-1 expression. Consistently, plasma GDF15 increased concurrently with C-peptide prior to the onset of chronic hyperglycemia in humans with pre-diabetes. In addition, in humans with T2D, exercise-induced GDF15 was associated with enhanced β-cell function. These findings support GDF15 as a potential therapeutic target for type 2 diabetes and associated co-morbidities.
2022-10-31 | GSE139872 | GEO
Project description:Living organisms are intricate systems with dynamic internal processes. Their RNA, protein, and metabolite levels fluctuate in response to variations in health and environmental conditions. Among these, RNA expression is particularly accessible for comprehensive analysis, thanks to the evolution of high throughput sequencing technologies in recent years. This progress has enabled researchers to identify unique RNA patterns associated with various diseases, as well as to develop predictive and prognostic biomarkers for therapy response. Such cross-sectional studies allow for the identification of differentially expressed genes (DEGs) between groups, but they have limitations. Specifically, they often fail to capture the temporal changes in gene expression following individual perturbations and may lead to significant false discoveries due to inherent noise in RNA sequencing sample preparation and data collection. To address these challenges, our study hypothesized that frequent, longitudinal RNA sequencing (RNAseq) analysis of blood samples could offer a more profound understanding of the temporal dynamics of gene expression in response to drug interventions, while also enhancing the accuracy of identifying genes influenced by these drugs. In this research, we conducted RNAseq on 829 blood samples collected from 84 Sprague-Dawley lab rats. Excluding the control group, each rat was administered one of four different compounds known for liver toxicity: tetracycline, isoniazid, valproate, and carbon tetrachloride. We developed specialized bioinformatics tools to pinpoint genes that exhibit temporal variation in response to these treatments.
2023-12-13 | GSE250058 | GEO