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

Insulin resistance is being recognized increasingly as the basis for the constellation of metabolic abnormalities that make up the metabolic syndrome, or Syndrome X. Insulin resistance is also the primary risk factor for the development of type 2 diabetes mellitus, which is currently reaching epidemic proportions by affecting more than 170 million people worldwide. A combination of environmental and genetic factors have led to a dramatic rise in visceral adiposity, the predominant factor causing insulin resistance and type 2 diabetes. Visceral adiposity is also the major risk factor for the development of Sleep Apnea (SA)--an association that has fueled interest in the co-morbidity of SA and the metabolic syndrome, but hampered attempts to ascribe an independent causative role for Sleep Apnea in the development of insulin resistance and type 2 diabetes. Numerous population and clinic-based epidemiologic studies have shown associations, often independent of obesity, between SA (or surrogates such as snoring) and measures of glucose dysregulation or type 2 diabetes. However, treatment of SA with continuous positive airway pressure (CPAP) has not been conclusive in demonstrating improvements in insulin resistance, perhaps due to the overwhelming effects of obesity. Here we show that in lean, otherwise healthy mice that exposure to intermittent hypoxia produced whole-body insulin resistance as determined by the hyperinsulinemic euglycemic clamp and reduced glucose utilization in oxidative muscle fibers, but did not cause a change in hepatic glucose output. Furthermore, the increase in insulin resistance was not affected by blockade of the autonomic nervous system. We conclude that intermittent hypoxia can cause acute insulin resistance in otherwise lean healthy animals, and the response occurs independent of activation of the autonomic nervous system.
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PMID:Metabolic consequences of intermittent hypoxia. 1826 87

Obesity has reached epidemic proportions in much of the industrialized world, and is also increasing in prevalence in the developing world. In the later decades of the 20th century until present, there have been numerous epidemiological studies reporting the relationship between excess weight and total, or all-cause, mortality. Obesity is associated with a wide variety of comorbidities such as type 2 diabetes, systemic hypertension, cardiovascular disease, certain cancers and sleep apnea, most of which may lead to disability or death. In general, the risk of developing comorbidities such as diabetes and cardiovascular disease rises as body mass index (BMI) increases. Using BMI, an indicator of relative weight for height (kg/m(2)) and a frequently used surrogate for assessing excess body fat, epidemiological studies have found linear, U- or J-shaped relationships between total mortality and BMI. However, obesity is remarkably heterogeneous. Obese patients considered to be 'at risk' are mostly characterized by features associated with the metabolic syndrome. The aim of the present paper is to review the cardiovascular consequences of obesity and to review some of the literature emphasizing why the cardiologist should measure other indices of adiposity in order to refine clinical assessment of obese individuals.
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PMID:Targeting abdominal obesity in cardiology: can we be effective? 1878 31

Sleep-disordered breathing and sleep apnoea are conditions frequently associated with comorbidity, including obesity, diabetes, hypertension, insulin resistance (metabolic syndrome) and cardiovascular disease. The diabetic state (type 1 and type 2 diabetes) may be associated to diminished lung function and, in particular, decreased vital capacity, and the association between chronic obstructive pulmonary disease (COPD) and type 2 diabetes may be due to a shared inflammatory process. Also, the alteration in circulating endothelial progenitor cells found in respiratory disease, the metabolic syndrome and cardiovascular disease reflect a common condition of endothelial dysfunction.
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PMID:The metabolic syndrome, diabetes and lung dysfunction. 1882 64

Metabolic syndrome is a disorder characterized by abdominal obesity, hypertension, increased triglycerides, decreased HDL cholesterol and increased blood glucose. Accumulating evidence strongly indicates that insulin resistance and an increased amount of abdominal fat are the pathogenic factors for the characteristics of metabolic syndrome. The metabolic syndrome is characterized by an increased risk for the development of cardiovascular disease and type 2 diabetes mellitus. Studies indicate that sleep apnea may be a manifestation of the metabolic syndrome. It has also been suggested that the metabolic syndrome or "syndrome X" should also comprise obstructive sleep apnea and should then be called syndrome "Z". It appears that obstructive sleep apnea and the metabolic syndrome are characterized by the same pathophysiologic environment, which increases the risk for the development of cardiovascular disease. The increased amount of visceral fat and the accompanying insulin resistance seem to be the main characteristics responsible for the development of obstructive sleep apnea and the metabolic syndrome.
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PMID:Metabolic syndrome and sleep apnea. 1892 60

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

The polycystic ovary syndrome (PCOS) affects 5-10% of women of child-bearing age, and the diagnosis carries with it associated metabolic and cardiovascular risk factors that are likely linked to insulin resistance. Consequently, women affected by PCOS are at significant risk for developing type 2 diabetes mellitus, cardiovascular disease, and obstructive sleep apnea. Aggressive screening for glucose intolerance and cardiovascular risk factors should be performed in all PCOS patients, and, when indicated by symptomatology, affected women should be screened for sleep apnea. Long-term goals of therapy should focus on prevention of these comorbidities.
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PMID:Comorbidities in polycystic ovary syndrome: their relationship to insulin resistance. 1907 70

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

Obesity is one of the greatest public health challenges of the 21st century with 1.6 billion adults currently classified as being overweight and 400 million as obese. Obesity is causally associated with type 2 diabetes, hypertension, cardiovascular disease, obstructive sleep apnoea and certain forms of cancer and is now one of the leading causes of mortality and morbidity worldwide. The gastrointestinal tract is the largest endocrine organ in the body producing hormones that have important sensing and signaling roles in regulating body weight and energy expenditure. The last decade has witnessed a marked increase in our understanding of the role of gut hormones in energy homeostasis. Consequently, strategies aimed at modulating circulating gut hormone concentrations or targeting their receptors are being developed as potential pharmacotherapies for obesity. This review summarizes the current knowledge regarding the mechanisms, sites of action and effects of the anorectic gut hormones peptide tyrosine-tyrosine (PYY), pancreatic polypeptide (PP), oxyntomodulin, and amylin and of the unique orexigenic hormone, ghrelin.
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PMID:The role of gut hormones in the regulation of body weight and energy homeostasis. 1956 62

Sleep-disordered breathing (SDB), especially sleep apnea-hypopnea syndrome, is often observed in patients with type 2 diabetes mellitus; but there are only a few studies on SDB in Japanese diabetic subjects. We investigated the prevalence of SDB in diabetic patients; associations between severity of sleep apnea (SA) and clinical factors, visceral fat, and adiponectin; and associations between type of SA and clinical factors. In the present study, 40 Japanese diabetic patients underwent overnight cardiorespiratory monitoring, and night and morning measurements of serum adiponectin concentrations. Sleep apnea was detected in Japanese diabetic patients at a high prevalence (77.5%). The following variables were associated with SDB: age, body mass index, estimated visceral fat area, and nocturnal reduction in serum adiponectin concentrations. The prevalence of central sleep apnea (CSA, >or=5/h) was 32.3% among diabetic SDB patients. Diabetic SDB patients with CSA had higher hemoglobin, increased intima-media thickness, and higher plasma brain natriuretic peptide levels than those without CSA (<5/h). In conclusion, our study demonstrated a high prevalence of SDB in Japanese diabetic patients, which correlated with visceral fat area and adiponectin. A high frequency of CSA was noted in diabetic SDB patients, together with high hemoglobin, high brain natriuretic peptide, and increased intima-media thickness. The present results of prevalence of SDB may be relevant to the higher incidence of cardiovascular disease in diabetic patients, which need to be clarified in future studies.
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PMID:Characteristics of sleep-disordered breathing in Japanese patients with type 2 diabetes mellitus. 1991 47

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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