Regulation of obesity and insulin resistance by hypoxia-inducible factors

Regulation of obesity and insulin resistance by hypoxia-inducible factors

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-...

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Bibliographic Details
Published in:Hypoxia Vol. 2; pp. 171 - 183
Main Authors: Ban, Jae-Jun, Ruthenborg, Robin J, Cho, Kevin W, Kim, Jung-Whan
Format: Journal Article Book Review
Language:English
Published: New Zealand Taylor & Francis Ltd 01-01-2014
Dove Medical Press
Subjects:
Adipocytes
Angiogenesis
Cancer
Diabetes
Gene expression
Hypoxia
Inflammation
Insulin resistance
Laparoscopy
Metabolic disorders
Nervous system
Obesity
Oxidative stress
Proteins
Review
Sleep apnea
Transcription factors
Tumor necrosis factor-TNF
inflammation
oxygen
hypoxia-inducible factor-1
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Summary: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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ObjectType-Review-1
ISSN:2324-1128
2324-1128
DOI:10.2147/hp.s68771