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Insulin resistance and adipose-derived hormones in young men with untreated obstructive sleep apnea
Authors:Trent A. Hargens  Stephen G. Guill  Anthony S. Kaleth  Sharon M. Nickols-Richardson  Larry E. Miller  Donald Zedalis  John M. Gregg  Frank Gwazdauskas  William G. Herbert
Affiliation:1. Department of Kinesiology, James Madison University, Harrisonburg, VA, 22807, USA
2. Laboratory for Health and Exercise Sciences, Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA
3. Department of Kinesiology, Indiana University-Purdue University, Indianapolis, IN, USA
4. Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA
5. Miller Scientific Consulting, Inc., 26 Portobello Road, Arden, NC, 28704, USA
6. Edward Via Virginia College of Osteopathic Medicine, Blacksburg, VA, USA
7. Health Research Group, LLC, Rockbridge Baths, VA, USA
8. Department of Dairy Science, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA
Abstract:

Purpose

Obstructive sleep apnea (OSA) increases the risk for insulin resistance (IR). The mechanisms that link the two are not clear and are frequently confounded by obesity. OSA is associated with alterations in adipose-derived hormones (adipokines) that increase IR; however, previous studies have focused on middle-aged and older adults. The objective of this study was to determine if IR and alterations in adipokines exist in young men with OSA, independent of obesity.

Methods

Subjects were assigned into the following groups based on body mass index and presence of OSA: obese with OSA (OSA, n?=?12), obese without OSA (NOSA, n?=?18), and normal weight without OSA (CON, n?=?15). Fasting blood was obtained for batch analysis of biomarkers of IR. The homeostasis model assessment (HOMA) method was used to assess IR.

Results

HOMA and leptin were higher in the OSA group than the CON group. There were no differences in insulin, tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) between the OSA and NOSA groups. Adiponectin was lower in the OSA group vs. NOSA and CON; however, when controlled for central abdominal fat (CAF), the difference was nullified. When controlled for total body adiposity, however, CAF was 24 % higher in the subjects with OSA vs. subjects without OSA.

Conclusions

These findings suggest that excess CAF in young men with OSA may contribute to risk for type 2 diabetes indirectly by a degree that would otherwise not be reached through obesity, although further research is needed.
Keywords:
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