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Ulysses J. Magalang, MD

The Ohio State University

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Director, OSU Sleep Disorders Program
Program Director, Sleep Medicine Fellowship Training Program

Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine
The Ohio State University
Room 201, Davis Heart and Lung Research Institute   
473 West 12th Street,  Columbus, OH 43017
Phone (614) 327 5579
email: magalang.1@osu.edu

Pubmed.com list of recent publications by Ulysses J. Magalang, M.D.

Research Area

My research is focused on the metabolic and cardiovascular effects of sleep disorders.

Current Research and Research Interests

Currently, we are examining the effects of intermittent hypoxia (IH), the main stimulus implicated in the health-related consequences of obstructive sleep apnea. Specifically, I am interested on the effects of IH on adipose tissue biology, particularly its effects on adiponectin, an adipocytokine with anti-inflammatory, anti-diabetic, and anti-atherogenic properties. I utilize a variety of models including cellular systems, animal models, and clinical research involving human subjects. We have shown for the first time that intermittent hypoxia reduces the secretion of both total and high-molecular-weight (the active form of the hormone) adiponectin by adipocytes. In our in vivo mouse model, the data shows that transgenic mice over-expressing adiponectin are protected from intermittent hypoxia-induced insulin resistance. Our preliminary study in humans showed for the first time that treatment of obstructive sleep apnea with CPAP for 3 months increased the levels of high-molecular weight adiponectin. Our group has published the first and only study that has utilized cardiac MRI to examine the effects of CPAP on cardiovascular remodeling.

In addition, through a collaborative effort with Dr. Philipp E. Scherer, who first described adiponectin, we have a published a seminal paper that showed that hypoxia, through activation of hypoxia-inducible factor 1 (HIF1 ) , fails to induce the expected pro-angiogenic response in adipose tissue, but rather HIF1 initiates adipose tissue fibrosis with an associated increase in local inflammation. Collectively, these observations are consistent with a model in which adipose tissue hypoxia serves as an early upstream initiator for adipose tissue dysfunction by inducing a local state of fibrosis. We have extended these findings in a polygenic animal model of Type 2 Diabetes Mellitus (Tally-Ho JngJ mouse) and our results indicate that IH mimicking the hypoxic stress seen in sleep apnea patients worsened glucose tolerance in the male Tally-Ho mice. This was associated with HIF1α stabilization, lysyl oxidase (LOX) activation, fibrosis, and macrophage infiltration in the visceral adipose tissue of TH mice, as well a decrease in circulating levels of the adipose-derived adiponectin indicating adipose tissue dysfunction. In addition, IH also induced pancreatic dysfunction likely related to an increase in circulating long chain unsaturated (palmitic and stearic) fatty acids.

Recently, I have been involved in the Sleep Apnea Genetics International Consortium. The mission of SAGIC is to enable research in the genetics and genomics of sleep apnea at an international level. This unique collaboration comprises international experts in the field of sleep research dedicated to further unraveling the genetics of sleep apnea and its associated co-morbidities. Collaborators of this consortium include sleep disorder and cardiovascular experts from the U.S., Iceland, Germany, France, Taiwan, Australia, and Brazil. In this consortium, I have completed a project examining the agreement of polysomnography scoring of respiratory events and sleep among international sleep centers. Our results suggest that centralized scoring of polysomnography may not be necessary in future research collaboration among the SAGIC centers.