University of Massachusetts Medical School Faculty Publications

UMMS Affiliation

Program in Molecular Medicine

Publication Date

10-17-2013

Document Type

Article

Subjects

Adipose Tissue; Animals; Disease Models, Animal; Humans; Insulin Resistance; Mice; Tumor Necrosis Factor-alpha

Disciplines

Cellular and Molecular Physiology | Endocrine System Diseases | Endocrinology

Abstract

Diet-induced obesity (DIO) predisposes individuals to insulin resistance, and adipose tissue has a major role in the disease. Insulin resistance can be induced in cultured adipocytes by a variety of treatments, but what aspects of the in vivo responses are captured by these models remains unknown. We use global RNA sequencing to investigate changes induced by TNF-alpha, hypoxia, dexamethasone, high insulin, and a combination of TNF-alpha and hypoxia, comparing the results to the changes in white adipose tissue from DIO mice. We found that different in vitro models capture distinct features of DIO adipose insulin resistance, and a combined treatment of TNF-alpha and hypoxia is most able to mimic the in vivo changes. Using genome-wide DNase I hypersensitivity followed by sequencing, we further examined the transcriptional regulation of TNF-alpha-induced insulin resistance, and we found that C/EPBbeta is a potential key regulator of adipose insulin resistance.

Rights and Permissions

Citation: Cell Rep. 2013 Oct 17;5(1):259-70. doi: 10.1016/j.celrep.2013.08.039. Epub 2013 Oct 3. Link to article on publisher's site

Comments

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Cell reports

PubMed ID

24095730

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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