Elsevier

Sleep Medicine

Volume 2, Issue 3, May 2001, Pages 207-213
Sleep Medicine

Original article
CPAP treatment does not affect glucose–insulin metabolism in sleep apneic patients

https://doi.org/10.1016/S1389-9457(00)00079-4Get rights and content

Abstract

Objective: We investigated glucose metabolism and insulin resistance in non-obese and moderately overweight sleep apnea patients, as well as their response to nasal CPAP treatment.

Methods: A group of subjects with glucose intolerance was screened for sleep disordered breathing by clinical interview and ambulatory recordings. Ten subjects were found to have untreated sleep apnea and were asked to participate in further investigation. This included nocturnal polysomnography, oral glucose tolerance test and indirect calorimetry. Subjects then had calibration of nasal CPAP with polysomnography. Two months after start of treatment, all subjects were restudied as at baseline. In parallel, six obstructive sleep apnea syndrome (OSAS) subjects, diagnosed through the sleep clinic, were matched for gender, age and oxygen desaturation index with the other group, and had a euglycemic hyperinsulinemic clamp at baseline and after 2 months of nasal CPAP.

Results: The first ten patients showed no change in total glucose oxidation, glucose oxidation by weight or by fat free mass, or insulin energetic expenditure, despite nocturnal usage of nasal CPAP. Similarly, when comparing baseline to the treatment at 2 months, the six OSAS patients had no change in mean glycemia, insulin, C peptide and hemoglobin (Hgb) A1C measurements. No difference in the amount of glucose infused during the duration of the clamp was noted either.

Conclusion: Our data do not support the existence of a significant relationship between glucose and insulin metabolism and obstructive sleep apnea. Obesity, when present, is the important variable.

Introduction

Obstructive sleep apnea is a common problem in the general population. Young et al. [1] studied a well-selected sample of 602 middle-aged patients (30–60 years old) and found that 24% of the men and 9% of the women had an apnea-hypopnea index >5 events/h of sleep. They estimated that 2% of women and 4% of men in the middle age work force meet the minimal diagnostic criteria for the sleep apnea syndrome (≥5 apnea-hypopnea events/ h of sleep and daytime hypersomnolence).

There are controversies surrounding the effects of obstructive sleep apnea and the repetitive short drops of oxygen saturation associated with the abnormal respiratory events on nocturnal glucose metabolism.

Previous studies [2], [3] have shown a relationship between glucose intolerance and obstructive sleep apnea syndrome (OSAS). High blood pressure, stroke and myocardial infarction have been associated with obstructive sleep apnea syndrome but also with insulin resistance [4], [5], [6]. The proposed mechanisms for the association between sleep disordered breathing and abnormal glucose metabolism included: presence of abnormal sympathetic activation, well demonstrated in OSAS patients [7], [8]; secondary development of atherosclerosis; and reduced endothelium-dependent vascular relaxation [9], [10]. Repetitive hypoxemia, with sympathetic activation and catecholamine release, contribute to insulin resistance [11], [12]. Based on these findings in obese OSA subjects, the possibility that abnormal breathing during sleep could be responsible for metabolic changes, and more particularly glucose intolerance and insulin resistance was considered [2], [3], [13]. Stoohs et al. [14], however, have argued against this position. Obesity is an important confounding variable, as it is associated with glucose intolerance and insulin resistance. Exclusion of clearly obese subjects when investigating the role of OSAS is one way to avoid the problems. Another strategy is to treat adequately the sleep apnea syndrome and to investigate any changes in glucose metabolism.

We designed a protocol that combined both approaches. We recruited non-obese or moderately overweight subjects with OSAS, including some with and some without glucose intolerance, and we investigated both subgroups at baseline and after 2 months of nasal CPAP treatment, with good nocturnal compliance.

Section snippets

Subjects

We recruited our subjects from the patient population consulting the endocrinology department at the University Hospital of Bordeaux. As part of their routine evaluation, all subjects had to complete a sleep questionnaire and undergo a clinical interview that included a sleep disorders evaluation. The sleep questionnaire included questions about snoring (frequency, loudness), observations by bed partners of abnormal breathing events during sleep and complaints of daytime tiredness and/or

For the ten subjects first recruited

The mean CPAP pressure was 6.4±1.08 cm H2O. Compared to baseline, during the night of CPAP titration, stage 1–2 decreased (ns), slow wave sleep increased (ns) as did REM sleep (ns). A significant augmentation trend was observed in sleep efficiency (P<0.02). The mean AHI significantly decreased (P<0.05) during the night of CPAP titration (from 31.06 to 3.1 events/h of sleep). The mean CPAP usage was 6.4±0.8 h/ day.

For the six matched OSAS patients

The mean CPAP pressure prescribed was 7.16±1.47 cm H2O. On the night of monitored

Discussion

The main goal of this study was to determine if a relationship between sleep, disordered breathing and glucose metabolism could be demonstrated. In order to limit bias factors regarding glucose metabolism, all our subjects came from a population of non-obese or moderately obese subjects. We carefully excluded patients with family history of diabetes [22], renal failure [23], hepatic insufficiency [24] or consumption of drugs interfering with glucose metabolism [25], such as beta blockers or

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      Repetitive hypoxias have been shown to cause insulin resistance (Braun et al., 2001) and the use of continuous positive airway pressure (CPAP) has been evaluated in OSA patients in relation with mortality (Campos-Rodriguez et al., 2012) and insulin sensitivity. Again the results are still conflicting: whereas some studies reported a better metabolic profile after CPAP treatment (Brooks et al., 1994; Lam et al., 2010; Sharma et al., 2011), other reports failed to identify improved insulin sensitivity (Smurra et al., 2001; West et al., 2007) or a reduction in blood pressure levels (Campos-Rodriguez et al., 2007; Iellamo and Montano, 2006). Regarding the prevalence of the individual MetS components in OSA patients, it is particularly high for hypertension and obesity.

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