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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With excess energy storage, obesity develops, leading to increased risk for type 2 diabetes and cardiovascular diseases. The distribution of body fat appears to be even more important than the total amount of fat. Abdominal and, in particular, visceral adiposity is strongly linked to insulin resistance, type 2 diabetes, hypertension, dyslipidaemia, sleep apnea, and other complications of obesity. Visceral adiposity, manifested as a high waist circumference, is now accepted as a major component of the metabolic syndrome. However, the biological mechanisms underlying the adverse impact of visceral fat accumulation remain to be established. This review will focus on the analysis of the biological specificity of adipose tissue located in the abdominal region, and will explore intervention strategies targeting the impaired function of the visceral adipocyte as potential therapies for the cardio-metabolic outcomes of patients with the metabolic syndrome.
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PMID:Biological specificity of visceral adipose tissue and therapeutic intervention. 1894 88

Obstructive sleep apnea is a common disorder in childhood, particularly in the last decade when an increased prevalence of obesity has been documented. The neurocognitive and behavioral problems associated with this disorder have been known for a long time. However, the increased knowledge of cardiovascular and metabolic complications in adults with sleep apnea has been followed by a better understanding of the systemic effects of upper airway obstruction in children. Obstructive sleep apnea (OSA) has been shown to induce autonomic imbalance in children and to affect blood pressure, cerebral blood flow and cardiac function in an early phase. OSA may also induce chronic systemic inflammation and may contribute to the development of metabolic syndrome in obese children. Very recent research indicates that in children primary snoring, the mildest form of the sleep-disordered breathing spectrum, may also be associated with morbidity. It is, therefore, likely that these respiratory sleep disorders do not simply influence children's' performance in private and social life, but may more seriously affect children's' health. The aim of this review is to outline early systemic complications of obstructive sleep apnea and primary snoring in infants and children.
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PMID:Pediatric sleep apnea: early onset of the 'syndrome'? 1905 83

Obstructive sleep apnoea (OSA) is associated with insulin resistance and metabolic syndrome. There is evidence that adipocyte-fatty acid binding protein (A-FABP) may be involved in the development of cardiometabolic dysfunction. The present authors hypothesise that A-FABP is upregulated in OSA. A total of 124 males without hypertension, diabetes mellitus, hyperlipidaemia or cardiovascular disease were recruited and underwent polysomnography. Serum A-FABP levels showed significant positive correlations with duration of oxygen desaturation and minimal oxygen saturation, fasting insulin and insulin resistance index by homeostasis model assessment. When subjects were divided into tertiles according to apnoea/hypopnoea index (AHI), serum A-FABP levels were significantly higher in the group with AHI >/=34.4 events.h(-1) than the groups with AHI 13.2-34.4 events.h(-1) or with AHI <13.2 events.h(-1). Serum A-FABP levels were significantly higher in the AHI >/=34.4 group than obesity-matched subjects with AHI <34.4 events.h(-1). Serum adipocyte-fatty acid binding protein levels correlated with obstructive sleep apnoea and insulin resistance, independently of obesity, and were significantly higher in severe obstructive sleep apnoea. Adipocyte-fatty acid binding protein may play a role in obstructive sleep apnoea and metabolic dysfunction.
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PMID:Serum adipocyte-fatty acid binding protein level is elevated in severe OSA and correlates with insulin resistance. 1918 13

Patients with obstructive sleep apnoea are at increased risk of atherosclerotic morbidity and mortality. Abnormalities in lipid metabolism that occur in response to chronic intermittent hypoxia in patients with sleep-disordered breathing may increase the cardiovascular risk in an already susceptible population. Atherogenic lipoprotein phenotype and small, dense LDL have an independent predictive role for future cardio- and cerebro-vascular events in patients with the metabolic syndrome. Therefore, testing the hypothesis that therapy of obstructive sleep apnoea may reduce atherogenic lipoprotein phenotype might have significant clinical implications. We suggest that abolition of obstructive sleep apnoea by continuous positive airway pressure results in reductions in circulatory levels of small, dense LDL by improvements in oxygen saturation, reductions in oxidative stress, improvements in insulin sensitivity, and reductions in triglyceride biosynthesis. Testing the proposed hypothesis may contribute to improvements in clinical management of patients with obstructive sleep apnoea by early recognition of atherogenic dyslipidaemia followed by both, vigorous treatment of the underlying sleep-disordered breathing by noninvasive ventilation and targeted therapeutic modulation of hypertriglyceridaemia, low HDL-cholesterol and increased levels of small, dense LDL. Implementing this strategy to patients with obstructive sleep apnoea may potentially contribute to substantial reduction of their high cardiovascular risk.
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PMID:Therapy with noninvasive ventilation in patients with obstructive sleep apnoea: effects on atherogenic lipoprotein phenotype. 1939 68

Recent attention has been drawn to the close association between obstructive sleep apnoea (OSA) and type 2 diabetes mellitus (T2DM). Debate has included much discussion about cause and effect with mechanisms proposed whereby one condition might cause the other. However, both clearly share a common phenotype, namely, obesity that overlaps considerably with the other components of the metabolic syndrome, hypertension and hyperlipidaemia. It would therefore appear likely that all are manifestations of the same basic pathological processes. Possible interacting aetiological mechanisms are reviewed along with treatment options. A recent report by the International Diabetes Federation has made recommendations to raise awareness of possible OSA in patients with T2DM and also for screening for hypertension, hyperlipidaemia and T2DM in patients with known OSA. The clinical implications are discussed.
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PMID:Obstructive sleep apnoea in patients with type 2 diabetes: aetiology and implications for clinical care. 1950 52

Sleep profoundly affects metabolic pathways. In healthy subjects, experimental sleep restriction caused insulin resistance (IR) and increased evening cortisol and sympathetic activation. Increased obesity in subjects reporting short sleep duration leads to speculation that, during recent decades, decreased sleeping time in the general population may have contributed to the increasing prevalence of obesity. Causal inference is difficult due to lack of control for confounders and inconsistent evidence of temporal sequence. In the general population, obstructive sleep apnoea (OSA) is associated with glucose intolerance. OSA severity is also associated with the degree of IR. However, OSA at baseline does not seem to significantly predict the development of diabetes. Prevalence of the metabolic syndrome is higher in patients with OSA than in obese subjects without OSA. Treatment with continuous positive airway pressure seems to improve glucose metabolism both in diabetic and nondiabetic OSA but mainly in nonobese subjects. The relative role of obesity and OSA in the pathogenesis of metabolic alterations is still unclear and is intensively studied in clinical and experimental models. In the intermittent hypoxia model in rodents, strong interactions are likely to occur between haemodynamic alterations, systemic inflammation and metabolic changes, modulated by genetic background. Molecular and cellular mechanisms are currently being investigated.
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PMID:Sleep, sleep-disordered breathing and metabolic consequences. 1988 Jun 25

The risks of metabolic syndrome and sleep-disordered breathing increase around the time of the menopause. We have previously shown that features of the nocturnal transcutaneous carbon dioxide (TcCO2) profile are associated with metabolic variables such as cholesterol, glycosylated haemoglobin A1C (GHbA1C) and blood pressure in patients with sleep apnoea. In the present study, we investigated whether these metabolic variables can be predicted using noninvasive TcCO2 measurements during sleep in generally healthy post-menopausal females. 22 post-menopausal females underwent an overnight polygraphic sleep study that involved the continuous monitoring of arterial oxygen saturation (S(a,O2)) and TcCO2. Body composition, GHbA1C, plasma cholesterol and blood pressure were measured prior to the sleep study. Nocturnal TcCO2 features were the most important predictors of lipoprotein cholesterols, triglycerides and blood pressure levels. A longer sleep period and higher TcCO2 levels were linked with lower GHbA1C, and fragmented sleep with lower high-density lipoprotein cholesterol. Neither nocturnal S(a,O2) indices nor the apnoea/hypopnoea index had a predictive power. The results suggest that nocturnal TcCO2 events revealed metabolic risk factors already present in healthy post-menopausal females.
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PMID:Transcutaneous carbon dioxide profile during sleep reveals metabolic risk factors in post-menopausal females. 1957 34

Obstructive sleep apnea (OSA) exerts several effects that may be particularly deleterious in patients with heart failure (HF). OSA should be considered especially in HF patients who are obese or have the metabolic syndrome, systemic hypertension, or pulmonary hypertension. HF patients in whom OSA is suspected should undergo a full evaluation by a sleep specialist, including a polysomnogram, to diagnose OSA and differentiate this disease from central sleep apnea. Those found to have OSA should then receive continuous positive airway pressure and/or other interventions, and standard disease management strategies should be used to maximize compliance. Those who cannot tolerate continuous positive airway pressure may be candidates for mandibular advancement devices or surgical therapies including tracheostomy. Standard HF medications should be used to treat HF, and optimization of fluid balance may help minimize OSA severity. However, it is still unknown whether treatment of OSA in HF patients will reduce hospitalizations or mortality.
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PMID:Obstructive sleep apnea and heart failure. 1993 Sep 82

During the past decades obesity and diabetes have become increasingly common in modern, industrialized societies. At the same time sleep disorders, chronic sleep loss and sleep deprivation have also become more and more prevalent. There may be a positive feed back circle between the two disorders: sleep problems may affect endocrine function and metabolic conditions, while metabolic abnormalities potentially interfere with sleep regulation. Sleep-disordered breathing, obstructive sleep apnea in particular, has the strongest association with glucose metabolism. Prevalence and severity of obstructive sleep apnea are higher among diabetic individuals compared to non-diabetic subjects. Central obesity is an important risk factor both in diabetes and sleep apnea, and recent evidence supports the direct association between them. Diabetic neuropathy and metabolic syndrome parameters correlate with the presence and severity of obstructive sleep apnea. Intermittent hypoxia may cause insulin resistance, consequently increasing the risk of diabetes and further impairing glycemic control. Specialists in both diabetology and sleep medicine need to work together to prevent the negative interactions between these two groups of disorders and to also preserve patients' quality of life and to improve outcomes.
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PMID:[Links between diabetes mellitus and sleep disorders: focusing on obstructive sleep apnea]. 2003 21

Over the past decade substantial evidence has accumulated implicating disorders of sleep in the pathogenesis of various metabolic abnormalities. This review, which is based on workshop discussions that took place at the 6th annual meeting of the International Sleep Disorders Forum: The Art of Good Sleep 2008 and a systematic literature search, provides a critical analysis of the available evidence implicating sleep disorders such as obstructive sleep apnoea (OSA), insomnia, short or long-term sleep duration and restless legs syndrome as potential risk factors for insulin resistance, glucose intolerance, type 2 diabetes mellitus and the metabolic syndrome. The review also highlights the evidence on whether treatment of specific sleep disorders can decrease metabolic risk. In total, 83 published reports were selected for inclusion. Although several studies show clear associations between sleep disorders and altered glucose metabolism, causal effects and the underlying pathophysiological mechanisms involved have not been fully elucidated. OSA appears to have the strongest association with insulin resistance, glucose intolerance, type 2 diabetes and the metabolic syndrome. There are, however, limited data supporting the hypothesis that effective treatment of sleep disorders, including OSA, has a favourable effect on glucose metabolism. Large randomized trials are thus required to address whether improvement of sleep quality and quantity can curtail excess metabolic risk. Research is also required to elucidate the mechanisms involved and to determine whether the effects of treatment for sleep disorders on glucose metabolism are dependent on the specific patient factors, the type of disorder and the duration of metabolic dysfunction. In conclusion, there is limited evidence on whether sleep disorders alter glucose metabolism and whether treatment can reduce the excess metabolic risk.
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PMID:Do sleep disorders and associated treatments impact glucose metabolism? 2004 48


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