What are the main mechanisms underlying the development of abnormal glucose metabolism in patients with OSA?
The hallmark of OSA is airflow reduction, which is typically associated with intermittent hypoxemia, sleep fragmentation, and SNS stimulation. In animal studies, insulin sensitivity has been shown to vary with intermittent hypoxemia, independent of activation of the SNS. Additionally, it has been shown that in overweight to mildly obese males without diabetes, every 4% decrease in oxygen saturation is associated with an odds ratio that approaches 2.0 for IGT. Sleep fragmentation has also been associated with abnormal glucose metabolism. In one study of healthy adults, selective suppression of SWS (without decreasing total sleep time) was associated with decreases in insulin sensitivity of nearly 25%! This suggests that the low levels of SWS in the sleep-restricted, the elderly, and obese subjects may contribute to their increased incidence of T2DM. In a study of consecutive adults with T2DM (age 41–77 years; BMI 20–57 kg/m 2 ), mild OSA was associated with a mean HbA 1c of 7.22% and severe OSA with a HbA 1c of almost 9.42%. After adjustments for age, gender, race, BMI, number of antidiabetes medications, level of exercise, years of diabetes, and total sleep time, the severity of OSA by AHI correlated significantly with higher mean HbA 1c values.