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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 9649608, 12 pages
https://doi.org/10.1155/2018/9649608
Research Article

Nocturnal Hypoxia Improves Glucose Disposal, Decreases Mitochondrial Efficiency, and Increases Reactive Oxygen Species in the Muscle and Liver of C57BL/6J Mice Independent of Weight Change

1Division of Endocrinology and Metabolism, University of Pittsburgh Medical Center, University of Pittsburgh, 3459 Fifth Avenue, 628 NW, Pittsburgh, PA 15213, USA
2Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, University of Pittsburgh, 3459 Fifth Avenue, 628 NW Pittsburgh, PA 15213, USA
3Department of Pharmacology and Chemical Biology, University of Pittsburgh Medical Center, University of Pittsburgh, 3459 Fifth Avenue, 628 NW Pittsburgh, PA 15213, USA

Correspondence should be addressed to Christopher P. O’Donnell; ude.cmpu@pcllennodo

Received 10 July 2017; Revised 14 November 2017; Accepted 29 November 2017; Published 4 February 2018

Academic Editor: Lena Lavie

Copyright © 2018 Simona Ioja et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Although acute exposure to hypoxia can disrupt metabolism, longer-term exposure may normalize glucose homeostasis or even improve glucose disposal in the presence of obesity. We examined the effects of two-week exposure to room air (Air), continuous 10% oxygen (C10%), and 12 hr nocturnal periods of 10% oxygen (N10%) on glucose disposal, insulin responsiveness, and mitochondrial function in lean and obese C57BL/6J mice. Both C10% and N10% improved glucose disposal relative to Air in lean and obese mice without evidence of an increase in insulin responsiveness; however, only the metabolic improvements with N10% exposure occurred in the absence of confounding effects of weight loss. In lean mice, N10% exposure caused a decreased respiratory control ratio (RCR) and increased reactive oxygen species (ROS) production in the mitochondria of the muscle and liver compared to Air-exposed mice. In the absence of hypoxia, obese mice exhibited a decreased RCR in the muscle and increased ROS production in the liver compared to lean mice; however, any additional effects of hypoxia in the presence of obesity were minimal. Our data suggest that the development of mitochondrial inefficiency may contribute to metabolic adaptions to hypoxia, independent of weight, and metabolic adaptations to adiposity, independent of hypoxia.