Unknown,Transcriptomics,Genomics,Proteomics

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Characterizing the profiles of histone markers in mouse adipocytes during insulin resistance


ABSTRACT: Insulin resistance is a sine qua non of Type 2 diabetes (T2D) and a frequent complication of multiple clinical conditions, including obesity, aging, and steroid use, among others. How such a panoply of insults can result in a common phenotype is incompletely understood. Furthermore, very little is known about the transcriptional and epigenetic basis of this disorder, despite evidence that such pathways are likely to play a fundamental role. Here, we compare cell autonomous models of insulin resistance induced by the cytokine tumor necrosis factor-a (TNF) or by the steroid dexamethasone (Dex) to construct detailed epigenomic maps associated with cellular insulin resistance. Murine 3T3-L1 adipocytes were treated separately with dexamethasone (Dex; 20nM) or tumor necrosis factor-alpha. To comprehensively assess epigenomic changes caused by Dex and TNF in a time-dependent manner, we profiled cells at early (2 hours), intermediate (24 hours), and late (6 days) points in the development of insulin resistance.

ORGANISM(S): Mus musculus

SUBMITTER: Evan Rosen 

PROVIDER: E-GEOD-58491 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Identification of nuclear hormone receptor pathways causing insulin resistance by transcriptional and epigenomic analysis.

Kang Sona S   Tsai Linus T LT   Zhou Yiming Y   Evertts Adam A   Xu Su S   Griffin Michael J MJ   Issner Robbyn R   Whitton Holly J HJ   Garcia Benjamin A BA   Epstein Charles B CB   Mikkelsen Tarjei S TS   Rosen Evan D ED  

Nature cell biology 20141215 1


Insulin resistance is a cardinal feature of Type 2 diabetes (T2D) and a frequent complication of multiple clinical conditions, including obesity, ageing and steroid use, among others. How such a panoply of insults can result in a common phenotype is incompletely understood. Furthermore, very little is known about the transcriptional and epigenetic basis of this disorder, despite evidence that such pathways are likely to play a fundamental role. Here, we compare cell autonomous models of insulin  ...[more]

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