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Hypoxia 2009 Speakers
Christopher O'Donnell
Division of Pulmonary Allergy and Critical Care Medicine, University of Pittsburgh, School of Medicine
Email: o'donnellcp@upmc.edu
Talk Title: Metabolic Consequences Of Intermittent Hypoxia
Session: Vascular, Metabolic, and Cognitive Effects of Intermittent Hypoxia
Abstract: Insulin resistance (IR) is being recognized increasingly as the basis for the constellation of metabolic abnormalities that make up the metabolic syndrome, or Syndrome X. Insulin resistance is also the primary risk factor for the development of type 2 diabetes mellitus (T2DM), which is currently reaching epidemic proportions by affecting more than 170 million people worldwide. A combination of environmental and genetic factors have led to a dramatic rise in visceral adiposity, the predominant factor causing IR and T2DB. Visceral adiposity is also the major risk factor for the development of Sleep Apnea - an association that has fueled interest in the co-morbidity of Sleep Apnea and the metabolic syndrome, but hampered attempts to ascribe an independent causative role for Sleep Apnea in the development of IR or T2DM. Numerous population and clinic-based epidemiologic studies have shown associations, often independent of obesity, between Sleep Apnea (or surrogates such as snoring) and measures of glucose dysregulation or T2DM. However, treatment of Sleep Apnea with continuous positive airway pressure (CPAP) has not been conclusive in demonstrating improvements in IR, perhaps due to the overwhelming effects of obesity or concomitant cytokine changes (e.g. leptin decreases, potentially opposing any beneficial effects of CPAP). Here we show that in lean, otherwise healthy mice that exposure to intermittent hypoxia produced whole-body IR as determined by the hyperinsulinemic euglycemic clamp, reduced glucose utilization in oxidative muscle fibers, but did not cause a change in hepatic glucose output. Furthermore, the increase in IR was not affected by blockade of the autonomic nervous system. We conclude that intermittent hypoxia can cause acute IR, in otherwise lean healthy animals, and the response occurs independent of activation of the autonomic nervous system.

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