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Type 2 diabetes mellitus is a systemic disease characterized by intolerance to glucose and peripheral resistance to insulin. This endocrine disease affects fundamental mechanisms of the central nervous system and jeopardizes the balance of vital functions such as the cardiovascular and circadian rhythm. The increased prevalence of metabolic disorders in our society is aggravated by endemic voluntary postponement of bedtime and by the current sedentary lifestyle, leading to epidemic proportions of obese people. Diabetes and chronic loss of sleep share the fact that both affect millions and one is detrimental to the other. Indeed, sleep deficits have marked modulatory effects on glucose metabolism and insulin sensitivity and foster metabolic syndrome that culminates in sleep disorders like restless syndrome and sleep apnea, which in turn lead to poor sleep quality. We examine the hypothesis that these two worldwide emerging disorders are due to two interlinked cycles. In our paradigm, we establish an intimate relationship between diabetes and sleep disturbances and postulate possible mechanisms that provide support for this conjecture. In addition, we propose some perspectives about the development of the reciprocal interaction between predictor components of metabolic syndrome and sleep disturbances that lead to poor sleep quality. The ability to predict the development and identify or associate a given mode of sleep disturbance to diabetes would be a valuable asset in the assessment of both. Furthermore, major advances in care coupled with healthy lifestyles can ensure a higher quality of life for people with diabetes.
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PMID:The reciprocal interaction between sleep and type 2 diabetes mellitus: facts and perspectives. 1806 Mar 21

The aim of the present study was to assess associations between obstructive sleep apnoea and insulin sensitivity in a population-based sample of females. In total, 400 females aged 20-70 yrs underwent a full-night polysomnography, fasting blood sampling, measurement of anthropometric variables and oral glucose tolerance test with measurement of the insulin response (n = 358). The apnoea/hypopnoea index (AHI) was calculated from the results of the polysomnography. From the results of the oral glucose tolerance test, an insulin sensitivity index (ISI) was calculated. Females with an AHI < 5 (n = 119) had a mean+/-SD ISI of 8.3+/-3.8, whereas females with an AHI > or = 30 (n = 34) had an ISI of 6.2+/-4.0. Nocturnal minimal saturation was independently associated with decreased insulin sensitivity when controlling for age, waist/hip ratio, level of physical activity, smoking and alcohol consumption (95% confidence interval (CI) 0.004-0.14). When adjusting for confounders, the AHI was associated with increased fasting and 2-h insulin levels (95% CI 0.14-0.99 and 95% CI 0.28-6.47, respectively). Obstructive sleep apnoea was found to be independently associated with decreased insulin sensitivity in the present population-based sample of females.
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PMID:Obstructive sleep apnoea is associated with decreased insulin sensitivity in females. 1818 81

Antioxidant counteraction of oxidative stress has been poorly explored in obstructive sleep apnoea (OSA). Serum albumin is a major antioxidant agent and structural modifications induced by glucose or free radicals impair its antioxidant properties. The aim of the present study was to compare antioxidant capacities and structural changes of albumin in nonobese OSA patients and healthy volunteers. Albumin structural changes were studied by quenching of fluorescence in the presence of acrylamide. Albumin thiols and fructosamines, reflecting oxidation- and glycation-induced changes in serum albumin, respectively, were assessed. Albumin structural changes were demonstrated by a significant decrease in quenching of fluorescence in OSA patients. Oxidation, resulting in a significant decrease in thiol groups (3.7+/-0.7 versus 2.3+/-0.4 micromol x g(-1) protein), and glycation, associated with a significant increase in fructosamines (226.6+/-27 versus 286+/-44.4 micromol x L(-1)), were found when comparing healthy volunteers with OSA patients. There was a significant relationship between both parameters and sleep apnoea severity. After continuous positive airway pressure intervention, albumin thiol groups were reassessed in seven of the 16 OSA patients and increased significantly from 2.25+/-0.39 to 2.79+/-0.31 micromol x g(-1) protein. Obstructive sleep apnoea patients demonstrated a reduction in serum albumin antioxidant properties that may aggravate oxidative stress and, thus, contribute to cardiovascular and metabolic morbidities.
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PMID:Impairment of serum albumin antioxidant properties in obstructive sleep apnoea syndrome. 1825 67

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

The reality of metabolic syndrome (MS) as a specific entity is debatable. However, the simple measure of waist circumference (>94 cm in men and >80 cm in women) is useful: (1) to check for insulin resistance by measuring serum levels of fasted glucose and insuline, cholesterol, triglycerides; (2) to look for diseases associated with MS such as hypertension, non alcohoolic steatohepatitis, sleep apnea, polycystic ovary disease, hypogonadism and to measure serum levels of ferritine, ALAT, ASAT, urate acid, CRP hs, testosterone and (3) to make obese people aware of their risk of becoming diabetic and to motivate them to change their life style. The utility of exercise and of various diets is discussed as well as the efficiency of drugs acting on different components of MS such as rimonabant, orlistat, metformin, glitazones, telmisartan and testosterone. The importance of political measures to fight the obesity epidemic is underlined.
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PMID:[Metabolic syndrome: jumble syndrome of obesity or specific entity? Which treatment: diet or polypill?]. 1838 74

The purpose of this study was to examine the possible difference in the 24-hr BP profile--including short-term BP variability, assessed as the standard deviation--between diabetic and non-diabetic hypertensives. We measured 24-hr ambulatory BP in 11 diabetic hypertensives (diabetic HT) and 10 non-diabetic hypertensives (non-diabetic HT) who were hospitalized for the educational program in our hospital and were under stable salt intake. Renal function and sleep apnea were also estimated. There were no significant differences in 24-hr systolic BP (141 mmHg vs. 135 mmHg, ns), daytime systolic BP (143 mmHg vs. 138 mmHg, ns), and nighttime systolic BP (135 mmHg vs. 130 mmHg, ns) between diabetic HT and non-diabetic HT. The values of 24-hr HR (69.7 beats/min vs. 65.2 beats/min, ns) and 24-hr HR variability (9.9 beats/min vs. 10.1 beats/min, ns) were also similar between the groups. Interestingly, diabetic HT had a significantly greater 24-hr systolic and diastolic BP variability than non-diabetic HT (18.2 mmHg vs. 14.5 mmHg, p < 0.05; 11.5 mmHg vs. 9.6 mmHg, p < 0.05, respectively). The values for creatinine clearance, urinary protein excretion, and apnea-hypopnea index were similar between the groups. Bivariate linear regression analysis demonstrated that fasting blood glucose was the primary determinant of 24-hr diastolic BP variability (r = 0.661, p < 0.01). Multiple stepwise regression analysis revealed that fasting blood glucose was a significant and independent contributor to 24-hr systolic BP variability (r = 0.501, p < 0.05). Taken together, these results demonstrate that BP variability is increased in diabetic hypertensives. Furthermore, it is possible that an elevation of fasting blood glucose may contribute to the enhanced BP variability in hypertensives.
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PMID:Ambulatory blood pressure variability is increased in diabetic hypertensives. 1842 1

Given the consequences of sleep apnea and coexisting diabetes, satisfactory treatment of both diseases is required. Our results of continuous glucose monitoring in severe sleep apnea diabetic patients before and during continuous positive airway pressure/CPAP therapy showed significant reduction of nocturnal glucose variability and improved overnight glucose control on CPAP.
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PMID:Beneficial effects of severe sleep apnea therapy on nocturnal glucose control in persons with type 2 diabetes mellitus. 1844 86

Obesity is known to be a major aetiological factor in the development of hypertension. It also leads to dyslipidaemia and raised blood glucose. All of these are components of the metabolic syndrome. Thus, hypertension, as part of the syndrome, is often found together with these other abnormalities. Obesity raises blood pressure by a number of mechanisms, including activation of the sympathetic nervous system and the renin- angiotensin system. Apart from cardiovascular disease and diabetes, the metabolic syndrome is also associated with fatty liver disease, sleep apnoea and some malignancies. Measures to reduce obesity through lifestyle changes are therefore highly desirable, not because of reductions in blood pressure alone.
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PMID:Hypertension as part of the metabolic syndrome. 1854 89

Acromegaly is an acquired disorder related to excessive production of growth hormone (GH) and characterized by progressive somatic disfigurement (mainly involving the face and extremities) and systemic manifestations. The prevalence is estimated at 1:140,000-250,000. It is most often diagnosed in middle-aged adults (average age 40 years, men and women equally affected). Due to insidious onset and slow progression, acromegaly is often diagnosed four to more than ten years after its onset. The main clinical features are broadened extremities (hands and feet), widened thickened and stubby fingers, and thickened soft tissue. The facial aspect is characteristic and includes a widened and thickened nose, prominent cheekbones, forehead bulges, thick lips and marked facial lines. The forehead and overlying skin is thickened, sometimes leading to frontal bossing. There is a tendency towards mandibular overgrowth with prognathism, maxillary widening, tooth separation and jaw malocclusion. The disease also has rheumatologic, cardiovascular, respiratory and metabolic consequences which determine its prognosis. In the majority of cases, acromegaly is related to a pituitary adenoma, either purely GH-secreting (60%) or mixed. In very rare cases, acromegaly is due to ectopic secretion of growth-hormone-releasing hormone (GHRH) responsible for pituitary hyperplasia. The clinical diagnosis is confirmed biochemically by an increased serum GH concentration following an oral glucose tolerance test (OGTT) and by detection of increased levels of insulin-like growth factor-I (IGF-I). Assessment of tumor volume and extension is based on imaging studies. Echocardiography and sleep apnea testing are used to determine the clinical impact of acromegaly. Treatment is aimed at correcting (or preventing) tumor compression by excising the disease-causing lesion, and at reducing GH and IGF-I levels to normal values. Transsphenoidal surgery is often the first-line treatment. When surgery fails to correct GH/IGF-I hypersecretion, medical treatment with somatostatin analogs and/or radiotherapy can be used. The GH antagonist (pegvisomant) is used in patients that are resistant to somatostatin analogs. Adequate hormonal disease control is achieved in most cases, allowing a life expectancy similar to that of the general population. However, even if patients are cured or well-controlled, sequelae (joint pain, deformities and altered quality of life) often remain.
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PMID:Acromegaly. 1857 66

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


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