Impaired Glucose Tolerance in Sleep Disorders

BACKGROUND: Recent epidemiological and experimental data suggest a negative influence of shortened or disturbed night sleep on glucose tolerance. Due to the high prevalence of sleep disorders this might be a major health issue. However, no comparative studies of carbohydrate metabolism have been conducted in clinical sleep disorders. METHODOLOGY/PRINCIPAL FINDINGS: We performed oral glucose tolerance tests (OGTT) and assessed additional parameters of carbohydrate metabolism in patients suffering from obstructive sleep apnea syndrome (OSAS, N = 25), restless legs syndrome (RLS, N = 18) or primary insomnia (N = 21), and in healthy controls (N = 33). Compared to controls, increased rates of impaired glucose tolerance were found in OSAS (OR: 4.9) and RLS (OR: 4.7) patients, but not in primary insomnia patients (OR: 1.6). In addition, HbA1c values were significantly increased in the same two patient groups. Significant positive correlations were found between 2-h plasma glucose values measured during the OGTT and the apnea-arousal-index in OSAS (r = 0.56; p<0.05) and the periodic leg movement-arousal-index in RLS (r = 0.56, p<0.05), respectively. Sleep duration and other quantitative aspects of sleep were similar between patient groups. CONCLUSIONS/SIGNIFICANCE: Our findings suggest that some, but not all sleep disorders considerably compromise glucose metabolism. Repeated arousals during sleep might be a pivotal causative factor deserving further experimental investigations to reveal potential novel targets for the prevention of metabolic diseases

No Impaired Glucose Tolerance in Primary Insomnia Patients with Normal Results of Polysomnography

BackgroundAccording to recent studies, sleep restriction and disruption both have a prominent negative influence on glucose metabolism. This could also be shown in sleep disorders, such as sleep apnea and the restless legs syndrome. However, similar studies regarding insomnia have not been that consistent, yet. Moreover, most previous studies did not include objective polysomnography (PSG) data.MethodsPatients with primary insomnia (N = 17) and healthy controls (N = 15) were investigated using psychometric tests such as the Epworth Sleepiness Scale and the Pittsburgh sleep quality index (PSQI). Two nights of full PSG were performed in all subjects, and after the first PSG night subjects underwent a standard oral glucose tolerance test (OGTT). PSG-, arousal-, and glucose metabolism-parameters were compared between groups.ResultsPatients with insomnia were, as expected, sleepier than healthy controls and showed higher PSQI values. All PSG parameters, however, including parameters related to nocturnal arousals, did not differ between groups. Moreover, OGGT results and all other parameters of glucose tolerance were not different between insomniac patients and healthy controls.ConclusionOur findings suggest that glucose tolerance is not impaired in patients with chronic insomnia and normal PSG-findings. Therefore, impaired glucose metabolism and diabetes related to insomnia in earlier studies might be restricted to those patients who have objectively disturbed sleep

Frequency of Patients with Normal Glucose Tolerance or Impaired Glucose Tolerance.

<p>Normal Glucose Tolerance: 2h-PG≤140 mg/dl; Impaired Glucose Tolerance: 2h-PG≥140 mg/dl.</p><p>OSAS, Obstructive sleep apnea syndrome; RLS, Restless legs syndrome; INS, Insomnia; CON, controls.</p><p>χ² (3) = 7.95, p<0.05.</p

Metabolic Parameters.

<p>Data are mean (SD). Statistical comparison was done using ANCOVA.</p><p>OSAS, Obstructive sleep apnea syndrome; RLS, Restless legs syndrome; INS, Insomnia; CON, controls; FPG = Fasting plasma glucose; FPI = Fasting plasma insulin; 2h-PG = 2h-Postload glucose; 2h-PI = 2h-Postload insulin; AUCg = Area under the curve for glucose; HOMA1-IR = Homeostasis model assessment-1 of insulin resistance; ISIcomposite = Insulin sensitivity index composite.</p><p>* p<0.05, † p<0.01, ‡ p<0.001.</p

Baseline Characteristics of Study Participants.

<p>Data are mean (SD). Statistical comparison was done using Gabriel- or Games-Howell-corrected oneway ANOVA.</p><p>OSAS, Obstructive sleep apnea syndrome; RLS, Restless legs syndrome; INS, Insomnia; CON, controls; BMI, Body mass index; PSQI, Pittsburgh Sleep Quality Index; ESS, Epworth Sleepiness Scale.</p><p>* p<0.05, † p<0.01, ‡ p<0.001, vs controls.</p><p>⁺ p<0.05, □ p<0.01, ∇ p<0.001, between groups.</p><p>OSAS: χ² (1) = 18.21, p<0.001; RLS: χ² (1) = 0.433, p>0.05; INS: χ² (1) = 0.163, p>0.05, vs controls.</p

Association between 2 hour-plasma glucose and the oxygen-desaturation-index in obstructive sleep apnea patients.

<p>Partial correlation coefficient (corrected for the BMI); r = 0.59, <i>p</i><0.05.</p

Frequency of Patients with Normal or Elevated HbA1c (≥5.5%) & FPG (≥100mg/dl).

<p>OSAS, Obstructive sleep apnea syndrome; RLS, Restless legs syndrome; INS, Insomnia; CON, controls; FPG = Fasting plasma glucose.</p><p>χ² (3) = 25·31, p<0·001.</p

Sleep Parameters.

<p>Data are mean (SD). Mean comparison was done using Gabriel- or Games-Howell-corrected oneway ANOVA.</p><p>OSAS, Obstructive sleep apnea syndrome; RLS, Restless legs syndrome; INS, Insomnia; CON, controls; TIB, Time in bed; TST, Total sleep time; SEI, Sleep efficiency; WASO, Wake time after sleep onset; REM, Rapid eye movement sleep; S1, Stage 1 sleep; S2, Stage 2 sleep, SWS, Slow wave sleep; SO, Sleep onset latency; SLREM, REM sleep latency; SLSWS, SWS sleep latency; AHI, Apnea-hypopnea-index; ODI, Oxygen-desaturation-index; PLMS-Index, Periodic leg movements per hour of sleep; PLMS-arousal-index, PLMS associated with arousals per hour of sleep; Apnea-arousal-index, Apneas and/or hypopneas associated with arousals per hour.</p><p>* p<0·05, † p<0·01, ‡ p<0·001.</p

Association between the 2 hour-plasma glucose and the PLMS-arousal-index in restless legs patients.

<p>Pearson's correlation coefficient; r = 0.56, <i>p</i><0.05.</p