Hypoxia, Oxidative Stress and Fat

Biomolecules

Nikolaus Netzer²  Hannes Gatterer²  Martin Faulhaber²  Martin Burtscher²  Stephan Pramsohler¹  Dominik Pesta²  Michael Breitenbach³ 

[1] Hermann Buhl Institute for Hypoxia and Sleep Medicine Research, Bad Aibling 83043, Germany; E-Mail:;Department of Sport Science, Faculty for Sports Science and Psychology, University of Innsbruck, Innsbruck 6020, Austria; E-Mails:Department of Sport Science, Faculty for Sports Science and Psychology, University of Innsbruck, Innsbruck 6020, Austria;

关键词: white adipose tissue;    adipocytes;    hypoxia;    oxidative stress;    cell metabolism;   

DOI  :  10.3390/biom5021143

来源: mdpi

【 摘 要 】

Metabolic disturbances in white adipose tissue in obese individuals contribute to the pathogenesis of insulin resistance and the development of type 2 diabetes mellitus. Impaired insulin action in adipocytes is associated with elevated lipolysis and increased free fatty acids leading to ectopic fat deposition in liver and skeletal muscle. Chronic adipose tissue hypoxia has been suggested to be part of pathomechanisms causing dysfunction of adipocytes. Hypoxia can provoke oxidative stress in human and animal adipocytes and reduce the production of beneficial adipokines, such as adiponectin. However, time-dose responses to hypoxia relativize the effects of hypoxic stress. Long-term exposure of fat cells to hypoxia can lead to the production of beneficial substances such as leptin. Knowledge of time-dose responses of hypoxia on white adipose tissue and the time course of generation of oxidative stress in adipocytes is still scarce. This paper reviews the potential links between adipose tissue hypoxia, oxidative stress, mitochondrial dysfunction, and low-grade inflammation caused by adipocyte hypertrophy, macrophage infiltration and production of inflammatory mediators.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.