Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of muscle insulin receptor knock-out mice treated with streptozotocin to induce diabetes


ABSTRACT: The targeted muscle insulin receptor knockout (MIRKO) model was used, in which there is a complete absence of the insulin-receptor signaling in skeletal muscle but normal insulin and glucose levels. By comparing skeletal muscle gene-expression profiles from MIRKO mice and their controls (lox/lox) under three different metabolic conditions (namely, in the basal state, after streptozotocin (STZ)-induced diabetes, and after STZ-induced diabetes rendered euglycemic with insulin treatment), we can address the following three important questions. (i) What is the direct effect of the loss of insulin signaling on gene expression in skeletal muscle? (ii) What is the contribution of the metabolic and other changes that accompany diabetes to induce indirect changes in gene expression? (iii) How are these pathways regulated and implicated in the pathophysiology of diabetes?

ORGANISM(S): Mus musculus

SUBMITTER: Ronald Kahn 

PROVIDER: E-CBIL-19 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Distinct pathways of insulin-regulated versus diabetes-regulated gene expression: an in vivo analysis in MIRKO mice.

Yechoor Vijay K VK   Patti Mary-Elizabeth ME   Ueki Kohjiro K   Laustsen Palle G PG   Saccone Robert R   Rauniyar Ravi R   Kahn C Ronald CR  

Proceedings of the National Academy of Sciences of the United States of America 20041116 47


Diabetes mellitus is a complex metabolic disorder accompanied by alterations in cellular physiology, metabolism, and gene expression. These alterations can be primary (due to loss of direct insulin action) or secondary (due to the metabolic perturbations associated with the disease). To dissect and quantitate these two separate effects, we compared the skeletal muscle gene-expression profiles of muscle insulin receptor knockout (MIRKO) mice and their Lox controls in the basal, streptozotocin-ind  ...[more]

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