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Alterations in Glucose Disposal in Sleep-disordered Breathing
Naresh M Punjabi1, Brock A Beamer
1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. npunjabi@jhmi.edu
Sleep-disordered breathing (SDB) significantly impairs insulin sensitivity and pancreatic beta-cell function, independent of body fat. These metabolic defects increase the risk for glucose intolerance and type 2 diabetes mellitus in individuals with SDB.
Area of Science:
- Metabolic research
- Sleep medicine
- Endocrinology
Background:
- Sleep-disordered breathing (SDB) is linked to insulin resistance, glucose intolerance, and type 2 diabetes.
- However, the direct impact of SDB on in vivo glucose and insulin kinetics remains unclear.
Purpose of the Study:
- To model in vivo glucose and insulin kinetics in individuals with and without SDB.
- To assess the effects of SDB on insulin sensitivity, glucose effectiveness, and pancreatic beta-cell function using minimal model analysis.
Main Methods:
- Utilized the frequently sampled intravenous glucose tolerance test (FSIVGTT) in 118 non-diabetic subjects.
- Polysomnography and body composition analysis were performed.
- Minimal model analysis derived key metabolic parameters.
Main Results:
- Reduced insulin sensitivity was observed in mild (26.7%), moderate (36.5%), and severe (43.7%) SDB groups, independent of body fat.
- Pancreatic beta-cell function (disposition index) was impaired in moderate to severe SDB.
- Insulin sensitivity and disposition index correlated with oxyhemoglobin desaturation; glucose effectiveness correlated with arousal frequency.
Conclusions:
- SDB is independently associated with impaired insulin sensitivity, glucose effectiveness, and beta-cell function, irrespective of adiposity.
- These metabolic dysfunctions contribute to an elevated risk of glucose intolerance and type 2 diabetes in SDB patients.
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