Abstract
BackgroundType 2 diabetes mellitus (T2DM) and obesity have become two of the main threats to public health in the Western world. In addition, obesity is the most important determinant of the sleep apnea-hypopnea syndrome (SAHS), a condition that adversely affects glucose metabolism. However, it is unknown whether patients with diabetes have more severe SAHS than non-diabetic subjects. The aim of this cross-sectional case-control study was to evaluate whether obese patients with T2DM are more prone to severe SAHS than obese non-diabetic subjects.Methodology/Principal FindingsThirty obese T2DM and 60 non-diabetic women closely matched by age, body mass index, waist circumference, and smoking status were recruited from the outpatient Obesity Unit of a university hospital. The exclusion criteria included chronic respiratory disease, smoking habit, neuromuscular and cerebrovascular disease, alcohol abuse, use of sedatives, and pregnancy. Examinations included a non-attended respiratory polygraphy, pulmonary function testing, and an awake arterial gasometry. Oxygen saturation measures included the percentage of time spent at saturations below 90% (CT90). A high prevalence of SAHS was found in both groups (T2DM:80%, nondiabetic:78.3%). No differences in the number of sleep apnea-hypopnea events between diabetic and non-diabetic patients were observed. However, in diabetic patients, a significantly increase in the CT90 was detected (20.2±30.2% vs. 6.8±13,5%; p = 0.027). In addition, residual volume (RV) was significantly higher in T2DM (percentage of predicted: 79.7±18.1 vs. 100.1±22.8; p<0.001). Multiple linear regression analyses showed that T2DM but not RV was independently associated with CT90.Conclusions/SignificanceT2DM adversely affects breathing during sleep, becoming an independent risk factor for severe nocturnal hypoxemia in obese patients. Given that SAHS is a risk factor of cardiovascular disease, the screening for SAHS in T2DM patients seems mandatory.
Highlights
Sleep apnea-hypopnea syndrome (SAHS) has been well established as an independent risk factor for hypertension, myocardial infarction, and stroke [1]
The cumulative percentage of time spent with oxygen saturation below 90% was three-fold higher in diabetes patients than in nondiabetic subjects matched by age, gender, BMI and waist circumference
This is an important finding because sleep related hypoxia in sleep apnea-hypopnea syndrome (SAHS) patients is known to be a major stimulus leading to oxidative stress and endothelial dysfunction [14], and may contribute to the increased risk of fatal and non-fatal cardiovascular events observed in patients with severe SAHS [1]
Summary
Sleep apnea-hypopnea syndrome (SAHS) has been well established as an independent risk factor for hypertension, myocardial infarction, and stroke [1]. The available data suggest that long-term exposure to intermittent hypoxia and sleep fragmentation increases sympathetic nerve activity, contributing to disorders of glucose metabolism [4] In this regard, a high prevalence of fasting hyperglucemia, insulin resistance, and T2DM has been found among SAHS patients in comparison with healthy subjects [5]. In non-obese rats, Ramadan et al [8] have recently shown direct evidence for the contribution of insulin resistance in the development of apneic episodes, and how treatment with metformin, a drug currently used to raise insulin sensitivity, reversed and prevented these episodes It is unknown whether or not diabetic patients have more severe apneic episodes than non-diabetic patients. Obesity is the most important determinant of the sleep apnea-hypopnea syndrome (SAHS), a condition that adversely affects glucose metabolism It is unknown whether patients with diabetes have more severe SAHS than non-diabetic subjects. The aim of this cross-sectional case-control study was to evaluate whether obese patients with T2DM are more prone to severe SAHS than obese non-diabetic subjects
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