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Gene Expression Profiles in Skeletal Muscle and Liver of Type 2 Diabetes Rats

ABSTRACT: Analyzing changes in gene expression in liver and skeletal muscle from streptozotocin-diabetic rats. From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P < 0.01) were identified in comparisons of skeletal muscle and liver, respectively. Interestingly, large numbers of DEGs (200) were common to both comparisons, which was clearly more than the predicted number (131 genes, P < 10−4). Further interpretation of gene ontology used three over-representation analysis software (WebGestalt, Expander and GATHER). All the tools detected one KEGG pathway (MAPK signaling) and two GO biological processes (response to stress and cell death), with enrichment of DEGs in both tissues. In addition, PPI (protein-protein interaction) networks constructed using human homologs not only revealed the tendency of DEGs to form a highly connected module, but also suggested a “hub” role of MAPK related genes (such as MAPK14) in the pathogenesis of T2D. Total RNA obtained from liver and skeletal muscle of streptozotocin-diabetic rats and controls, respectivly.

ORGANISM(S): Rattus norvegicus

SUBMITTER: xl tang

PROVIDER: E-GEOD-41832 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene Expression Profiles in Skeletal Muscle and Liver of Type 2 Diabetes Rats

Project description:Analyzing changes in gene expression in liver and skeletal muscle from streptozotocin-diabetic rats. From the 9,929 expressed genes across the genome, 1,305 and 997 differentially expressed genes (DEGs, P < 0.01) were identified in comparisons of skeletal muscle and liver, respectively. Interestingly, large numbers of DEGs (200) were common to both comparisons, which was clearly more than the predicted number (131 genes, P < 10−4). Further interpretation of gene ontology used three over-representation analysis software (WebGestalt, Expander and GATHER). All the tools detected one KEGG pathway (MAPK signaling) and two GO biological processes (response to stress and cell death), with enrichment of DEGs in both tissues. In addition, PPI (protein-protein interaction) networks constructed using human homologs not only revealed the tendency of DEGs to form a highly connected module, but also suggested a “hub” role of MAPK related genes (such as MAPK14) in the pathogenesis of T2D.

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