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Regulation of obesity and insulin resistance by hypoxia-inducible factors

Authors Ban J, Ruthenborg R, Cho K, Kim J

Received 3 June 2014

Accepted for publication 25 July 2014

Published 13 November 2014 Volume 2014:2 Pages 171—183

DOI https://doi.org/10.2147/HP.S68771

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 5

Editor who approved publication: Prof. Dr. Dörthe Katschinski


Jae-Jun Ban, Robin J Ruthenborg, Kevin W Cho, Jung-whan Kim

Department of Biological Sciences, The University of Texas at Dallas, Richardson, TX, USA

Abstract: In obesity, dysregulated metabolism and aberrant expansion of adipose tissue lead to the development of tissue hypoxia that plays an important role in contributing to obesity-associated metabolic disorders. Recent studies utilizing adipocyte-specific hypoxia-inducible factor-α (HIF-α) gain- or loss-of-function animal models highlight the pivotal involvement of hypoxic responses in the pathogenesis of obesity-associated inflammation and insulin resistance. HIF-1α, a master transcription factor of oxygen homeostasis, induces inflammation and insulin resistance in obesity, whereas its isoform, HIF-2α, exerts opposing functions in these obesity-associated metabolic phenotypes. In this review, recent evidence elucidating functional implications of adipocyte HIFs in obesity and, more importantly, how these regulate obesity-associated inflammation, fibrosis, and insulin resistance will be discussed. Further, we propose that modulation of HIF-1 could be a potential novel therapeutic strategy for antidiabetic treatment.

Keywords: hypoxia-inducible factor-1, inflammation, oxygen
 

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