Obstructive Sleep Apnea and Diabetes: A State of the Art Review

Abstract

OSA is a chronic treatable sleep disorder and a frequent comorbidity in patients with type 2 diabetes. Cardinal features of OSA, including intermittent hypoxemia and sleep fragmentation, have been linked to abnormal glucose metabolism in laboratory-based experiments. OSA has also been linked to the development of incident type 2 diabetes. The relationship between OSA and type 2 diabetes may be bidirectional in nature given that diabetic neuropathy can affect central control of respiration and upper airway neural reflexes, promoting sleep-disordered breathing. Despite the strong association between OSA and type 2 diabetes, the effect of treatment with CPAP on markers of glucose metabolism has been conflicting. Variability with CPAP adherence may be one of the key factors behind these conflicting results. Finally, accumulating data suggest an association between OSA and type 1 diabetes as well as gestational diabetes. This review explores the role of OSA in the pathogenesis of type 2 diabetes, glucose metabolism dysregulation, and the impact of OSA treatment on glucose metabolism. The association between OSA and diabetic complications as well as gestational diabetes is also reviewed.

Keywords: OSA; central sleep apnea; diabetic complications; gestational diabetes; sleep apnea; type 1 diabetes; type 2 diabetes; weight loss.

Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1

Laboratory-based experiments assessing changes in insulin sensitivity following sleep manipulations in healthy human subjects. HOMA= homeostasis model assessment; IVGTT= intravenous glucose tolerance test, OGTT= oral glucose tolerance test; SWS= slow wave sleep. Modified with permission from Reutrakul and Van Cauter.

Figure 2

Mechanistic pathways linking OSA to diabetes. HPA = hypothalamic–pituitary–adrenal.

Figure 3

Relative risk of incident diabetes from prospective cohort studies in those with OSA compared with those without OSA. A, Unadjusted pooled relative risk. B, Adjusted pooled relative risk.

Figure 4

OSA prevalence in studies of patients with type 2 diabetes. In the study by Resnick et al and Einhorn et al, the moderate OSA column includes moderate and severe OSA.

Figure 5

Prospective studies examining the independent association between OSA severity and glycemic control assessed by HbA1c in type 2 diabetes. HbA1c has been adjusted for important confounders and represents the difference between severe OSA and no/mild OSA. In the study by Grimaldi et al, the highest quartile of the apnea-hypopnea index (AHI) during rapid eye movement (REM) sleep was compared with the lowest quartile or REM AHI. The mean total AHI in the highest quartile of REM AHI was 47 events/h. In contrast, the mean total AHI in the lowest quartile of REM AHI was 9 events/h. HbA1c = hemoglobin A1c.