Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to examine the existence of increased arterial stiffness of the central to middle-sized arteries and left ventricular (LV) structural/functional abnormalities in subjects with obstructive sleep apnea (OSA) who had normal clinic blood pressure. Brachial-ankle pulse wave velocity (baPWV) measurement and echocardiography were conducted in 164 consecutive subjects with normal clinic blood pressure evaluated for sleep disorders. Multivariate linear regression analysis showed that the apnea-hypopnea index (AHI) was an independently associated variable, even after adjustments for age, gender and risk factors for cardiovascular disease, with baPWV (R(2)=0.39, beta=0.19, P<0.01) and the E/A ratio (R(2)=0.51, beta=-0.27, P<0.01). The baPWV and LV relative wall thickness at diastole (RWTd) were significantly higher (P<0.05), and the E/A ratio was significantly lower (P<0.05), in subjects with severe OSA (AHI> or =30 episodes per hour) than in non-OSA subjects (AHI<5 episodes per hour). The analysis also showed that the baPWV bore a significant independent relationship to the RWTd (beta=0.19, P=0.02) and E/A ratio (beta=-0.12, P=0.04) adjusted for the risk factors for cardiovascular disease, the presence of metabolic syndrome and the severity of OSA. Thus, in this study, we showed the existence of increased arterial stiffness of the central to middle-sized arteries and LV structural/functional abnormalities in severe OSA patients, even in subjects with normal clinic blood pressure, suggesting the possible existence of a direct association between OSA and cardiovascular abnormalities.
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PMID:Concomitant existence and interaction of cardiovascular abnormalities in obstructive sleep apnea subjects with normal clinic blood pressure. 1926 83

This paper provides a review of literature on the effects of shift work on physical health, mental health and well-being. In Europe, 20% of the workforce is involved in irregular work schedules. Up to 70% of workers report problems, with increasing age, associated with more difficulties in adjusting to shift work. Epidemiologic studies on large populations have suggested a relation between employment in shift work and the incidence of sleep disorders, cancer, cardiovascular disease, diabetes, obesity, metabolic syndrome, reduced fecundity, preterm births, low birth weight, spontaneous abortion, work and traffic accidents, etc. Shift work exerts major influences on the physiological functions of the human body, mediated by the disruption of circadian rhythms.
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PMID:[Morbidity of irregular work schedules]. 1989 78

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

The histamine H(3) receptor is involved in the central and peripheral regulation of levels of histamine and other neurotransmitters (e.g., acetylcholine, noradrenaline, dopamine, serotonin and GABA), which sets it up as a target in the treatment of various CNS (e.g., depression, schizophrenia, ADHD, dementia, neuropathic pain and sleep disorders), metabolic syndrome (e.g., obesity) and allergic disorders. Novel chemical series from the most recent 2 years of patent literature have been reviewed. While overall structural diversity is moderate, these represent or relate to some of the compounds progressing through clinical trials (e.g., GSK-189254). However, an H(3) receptor drug still has yet to reach the market. Patenting activity is likely to remain high in the near future, bolstered by the commercial promise of potential H(3) receptor drugs.
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PMID:Recent advances in the development of histamine H3 antagonists. 2014 64

Metabolic syndrome (MS) patients exhibit sleep/wake disturbances and other circadian abnormalities, and these may be associated with more rapid weight increase and development of diabetes and atherosclerotic disease. On this basis, the successful management of MS may require an ideal drug that besides antagonizing the trigger factors of MS could also correct the disturbed sleep-wake rhythm. Melatonin is an effective chronobiotic agent able to change the phase and amplitude of circadian rhythms. Melatonin has also significant cytoprotective properties preventing a number of MS sequelae in animal models of diabetes and obesity. A small number of controlled trials indicate that melatonin is useful to treat the metabolic and cardiovascular comorbidities of MS. Whether the recently introduced melatonergic agents (ramelteon, agomelatine, tasimelteon) have the potential for treating sleep disorders in MS patients and, more generally, for arresting the progression of disease, merits further investigation.
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PMID:Melatonin and the metabolic syndrome: physiopathologic and therapeutical implications. 2135 75

Sleep disorders, sleep fragmentation, and chronically reduced sleep duration are increasingly common in western societies. In parallel, incidence of the metabolic syndrome and its key components, i.e. type 2 diabetes and obesity, is rapidly increasing. A huge number of epidemiological studies has shown a robust association between disturbed sleep quality, reduced sleep duration and the development of components of the metabolic syndrome. Moreover, there is growing evidence from experimental studies proving a causal link between sleep loss and disturbed human energy homeostasis. Short term sleep loss has been shown to reduce insulin sensitivity and glucose tolerance, increase feelings of hunger by modulating orexigenic/anorexigenic hormonal signaling, and disturb physical activity behavior. This review attempts to present an overview of the presently available literature on the link between sleep loss and disturbed human energy homeostasis, as well as on potential pathophysiological mechanisms.
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PMID:[Disturbed sleep as risk factor for metabolic syndrome]. 2142 44

Shift work is a fundamental component of the US workforce and an integral part of the lifestyles of a large proportion of the population. More than 22 million Americans work on shifts as part of their work life. Emerging research suggests that shift workers are at higher risk for a range of metabolic disorders and diseases (eg, obesity, cardiovascular disease, peptic ulcers, gastrointestinal problems, abnormal blood glucose levels, and metabolic syndrome). Sleep disorders associated with shift work also pose a serious public health risk, as they can impair an individual's ability to perform effectively and may lead to occupational and traffic accidents.
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PMID:Shift work and sleep: optimizing health, safety, and performance. 2153 97

Essential hypertension, insulin resistance, heart failure, congestion, diuretic resistance, and functional renal disease are all characterized by excessive central sympathetic drive. The contribution of the kidney's somatic afferent nerves, as an underlying cause of elevated central sympathetic drive, and the consequences of excessive efferent sympathetic signals to the kidney itself, as well as other organs, identify the renal sympathetic nerves as a uniquely logical therapeutic target for diseases linked by excessive central sympathetic drive. Clinical studies of renal denervation in patients with resistant hypertension using an endovascular radiofrequency ablation methodology have exposed the sympathetic link between these conditions. Renal denervation could be expected to simultaneously affect blood pressure, insulin resistance, sleep disorders, congestion in heart failure, cardiorenal syndrome and diuretic resistance. The striking epidemiologic evidence for coexistence of these disorders suggests common causal pathways. Chronic activation of the sympathetic nervous system has been associated with components of the metabolic syndrome, such as blood pressure elevation, obesity, dyslipidemia, and impaired fasting glucose with hyperinsulinemia. Over 50% of patients with essential hypertension are hyperinsulinemic, regardless of whether they are untreated or in a stable program of treatment. Insulin resistance is related to sympathetic drive via a bidirectional mechanism. In this manuscript, we review the data that suggests that selective impairment of renal somatic afferent and sympathetic efferent nerves in patients with resistant hypertension both reduces markers of central sympathetic drive and favorably impacts diseases linked through central sympathetics-insulin resistance, heart failure, congestion, diuretic resistance, and cardiorenal disorders.
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PMID:Sympatho-renal axis in chronic disease. 2168 96

Corticosteroids constitute an ideal treatment for various inflammatory and autoimmune disorders due to their anti-inflammatory and immunomodulatory actions. However, corticosteroids have a considerable number of side effects, including hypertension, diabetes, lipid disorders, sleep apnea, osteoporosis, myopathy, and disorders of coagulation and fibrinolysis, which are components of Cushing's syndrome (CS). Corticosteroid-induced side effects are dependent on the formulation, route, dose, and time of exposure. However, the underlying pathogenetic mechanisms have not been clearly defined. A large body of evidence supports the role of an imbalance between vasoconstriction and vasodilation with possible links to nitric oxide, prostanoids, angiotensin II, arginine vasopressin, endothelins, catecholamines, neuropeptide Y, and atrial natriuretic peptide. Increased oxidative stress, renin-angiotensin system activation, increased pressor response, metabolic syndrome, and sleep apnea appear to be pathogenetically involved as well. The ideal treatment is the withdrawal of corticosteroids, which is most often impossible due to the exacerbation of the underlying disease. Alternatively, a careful plan, including the proper selection of the formulation, time, and route, should be made, and each side effect should be treated properly. The focus of the research should be to develop synthetic corticosteroids with anti-inflammatory effects but fewer metabolic effects, which so far has been unsuccessful.
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PMID:Hypertension and other morbidities with Cushing's syndrome associated with corticosteroids: a review. 2194 34


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