Background: The effects of continuous positive airway pressure (CPAP) for obstructive sleep apnoea (OSA) on insulin resistance are not clear. Trials have found conflicting results and no appropriate control groups have been used. Methods: Forty-two men with known type 2 diabetes and newly diagnosed OSA (.10 dips/h in oxygen saturation of .4%) were randomised to receive therapeutic (n = 20) or placebo CPAP (n = 22) for 3 months. Baseline tests were performed and repeated after 3 months. The study was double blind. Results: Results are expressed as mean (SD). CPAP improved the Epworth sleepiness score significantly more in the therapeutic group than in the placebo group (26.6 (4.5) vs 22.6 (4.9), p = 0.01). The maintenance of wakefulness test improved significantly in the therapeutic group but not in the placebo group (+10.6 (13.9) vs 24.7 (11.8) min, p = 0.001). Glycaemic control and insulin resistance did not significantly change in either the therapeutic or placebo groups: HbA1c (20.02 (1.5) vs +0.1 (0.7), p = 0.7, 95% CI 20.6% to +0.9%), euglycaemic clamp (M/I: +1.7 (14.1) vs 25.7 (14.8), p = 0.2, 95% CI 21.8 to +0.3 l/kg/min 1000 ), HOMA-%S (21.5 (2.3) vs 21.1 (1.8), p = 0.2, 95% CI 20.3% to +0.08%) and adiponectin (21.1 (1.2) vs 21.1 (1.3), p = 0.2, 95% CI 20.7 to +0.6 mg/ml). Body mass index, bioimpedance and anthropometric measurements were unchanged. Hours of CPAP use per night were 3.6 (2.8) in the treatment group and 3.3 (3.0) in the placebo group (p = 0.8). There was no correlation between CPAP use and the measures of glycaemic control or insulin resistance. Conclusion: Therapeutic CPAP does not significantly improve measures of glycaemic control or insulin resistance in men with type 2 diabetes and OSA.

Background: A study was undertaken to establish the prevalence of obstructive sleep apnoea (OSA) in men with type 2 diabetes. Methods: Men with type 2 diabetes from local hospital and selected primary care practitioner databases received questionnaires about snoring, apnoeas, and daytime sleepiness based on the Berlin questionnaire. Selected respondents had overnight oximetry to establish whether they had OSA. Comparisons of oximetry were made with those from a previous general population study. HbA1c results were collected. Results: 1682 men were sent questionnaires, 56% of whom replied. 57% scored as ''high'' and 39% as ''low'' risk for OSA; 4% were already known to have OSA. Oximetry was performed in 240 respondents from both risk groups: 31% of the ''high'' and 13% of the ''low'' risk group had significant OSA (more than 10 .4% SaO 2 dips/hour or SaO 2 tracing consistent with OSA). These results were verified by detailed sleep studies. Extrapolation of the oximetry data to the questionnaire respondent population suggests that 23% had OSA. Comparison of the oximetry results with men from a previous general population study (using only more than 10 .4% SaO 2 dips/hour to define OSA) showed the prevalence of OSA is significantly higher in this diabetes population (17% v 6%, p,0.001). Multiple linear regression revealed BMI and diabetes as significant independent predictors of OSA. Following correction for BMI (which explained 13% of the variance in OSA), diabetes explained a further 8% of the variance (p,0.001). There was a low correlation between OSA severity and HbA1c in the subgroup recruited from the hospital database (r = 0.2, p = 0.006) which remained significant after allowing for obesity (p = 0.03). Conclusions: OSA is highly prevalent in men with type 2 diabetes; most are undiagnosed. Diabetes itself may be a significant independent contributor to the risk of OSA.

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In patients with minimally symptomatic OSA, diverse properties of endothelial function are impaired and arterial stiffness is increased. Although this was not associated with a significantly increased ABP, the findings suggest that patients with minimally symptomatic OSA are at increased cardiovascular risk.

In men with Type 2 diabetes, there is a strong association between retinopathy and OSA, independent of conventional retinopathy risk factors.

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Moderate-severe obstructive sleep apnoea (OSA) has been associated with several pro-atherogenic mechanisms and increased cardiovascular risk, but it is not known if minimally symptomatic OSA has similar effects. Circulating cell-derived microparticles have been shown to have pro-inflammatory, pro-coagulant and endothelial function-impairing effects, as well as to predict subclinical atherosclerosis and cardiovascular risk.In 57 patients with minimally symptomatic OSA, and 15 closely matched control subjects without OSA, AnnexinV-positive, platelet-, leukocyte-and endothelial cell-derived microparticles were measured by flow cytometry.In patients with OSA, median (interquartile range) levels of AnnexinV-positive microparticles were significantly elevated compared with control subjects: 2,586 (1,566-3,964) mL -1 versus 1,206(474-2,501) mL -1 , respectively. Levels of platelet-derived and leukocyte-derived microparticles were also significantly higher in patients with OSA (2,267 (1,102-3,592) mL -1 and 20 (14-31) mL -1 , respectively) compared with control subjects (925 (328-2,068) mL -1 and 15 (5-23) mL -1 , respectively). Endothelial cell-derived microparticle levels were similar in patients with OSA compared with control subjects (13 (8-25) mL -1 versus 11 (6-17) mL -1 ).In patients with minimally symptomatic obstructive sleep apnoea, levels of AnnexinV-positive, platelet-and leukocyte-derived microparticles are elevated when compared with closely matched control subjects without obstructive sleep apnoea. These findings suggest that these patients may be at increased cardiovascular risk, despite being minimally symptomatic.

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