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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep disorders are common in humans, and sleep loss increases the risk of obesity and diabetes. Studies in Drosophila have revealed molecular pathways and neural tissues regulating sleep; however, genes that maintain genetic variation for sleep in natural populations are unknown. Here, we characterized sleep in 40 wild-derived Drosophila lines and observed abundant genetic variation in sleep architecture. We associated sleep with genome-wide variation in gene expression to identify candidate genes. We independently confirmed that molecular polymorphisms in Catsup (Catecholamines up) are associated with variation in sleep and that P-element mutations in four candidate genes affect sleep and gene expression. Transcripts associated with sleep grouped into biologically plausible genetically correlated transcriptional modules. We confirmed co-regulated gene expression using P-element mutants. Quantitative genetic analysis of natural phenotypic variation is an efficient method for revealing candidate genes and pathways.
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PMID:Co-regulated transcriptional networks contribute to natural genetic variation in Drosophila sleep. 1923 72

Pneumologists frequently see obese and diabetic patients because of the high prevalence of these pathologies associated with sleep apneas. Nevertheless, the search for a sleep apnea syndrome is sometimes negative and the pneumologist is faced with unexplained complaints of sleepiness and sleep disorders. Pneumologists have to be familiar with and explore other nonrespiratory disorders in order to improve patient care. Inflammatory mechanisms have been suspected in several recent studies on daytime sleepiness. Sleep duration, obesity and diabetes are supposed to be linked because of hormonal modifications induced by sleep deprivation. Moreover, a relationship between diabetes and restless legs syndrome is not excluded.
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PMID:[Nonrespiratory sleep disorders in obese and diabetic patients]. 1937 45

Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder leading to cardiovascular and metabolic complications. OSA is also a multicomponent disorder, with intermittent hypoxia (IH) as the main trigger for the associated cardiovascular and metabolic alterations. Indeed, recurrent pharyngeal collapses during sleep lead to repetitive sequences of hypoxia-reoxygenation. This IH induces several consequences such as hemodynamic, hormonometabolic, oxidative, and immuno-inflammatory alterations that may interact and aggravate each other, resulting in artery changes, from adaptive to degenerative atherosclerotic remodeling. Atherosclerosis has been found in OSA patients free of other cardiovascular risk factors and is related to the severity of nocturnal hypoxia. Early stages of artery alteration, including functional and structural changes, have been evidenced in both OSA patients and rodents experimentally exposed to IH. Impaired vasoreactivity with endothelial dysfunction and/or increased vasoconstrictive responses due to sympathetic, endothelin, and renin-angiotensin systems have been reported and also contribute to vascular remodeling and inflammation. Oxidative stress, inflammation, and vascular remodeling can be directly triggered by IH, further aggravated by the OSA-associated hormonometabolic alterations, such as insulin resistance, dyslipidemia, and adipokine imbalance. As shown in OSA patients and in the animal model, genetic susceptibility, comorbidities (obesity), and life habits (high fat diet) may aggravate atherosclerosis development or progression. The intimate molecular mechanisms are still largely unknown, and their understanding may contribute to delineate new targets for prevention strategies and/or development of new treatment of OSA-related atherosclerosis, especially in patients at risk for cardiovascular disease.
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PMID:Obstructive sleep apnea, immuno-inflammation, and atherosclerosis. 1940 44

Evidences indicate that a complex relationship exists among sleep disorders, obesity and insulin resistance. NEU-P11 is a novel melatonin agonist used in treatment of psychophysiological insomnia, and in animal studies NEU-P11 showed sleep-promoting effect. In this study, we applied NEU-P11 on obese rats to assess its potential melatoninergic effects in vivo. Obese models were established using high-fat/high-sucrose-fed for 5 months. NEU-P11 (10mg/kg)/melatonin (4mg/kg)/vehicle were administered by a daily intraperitoneal injection respectively for 8 weeks. Our results showed that NEU-P11 or melatonin inhibited both body weight gain and deposit of abdominal fat with no influence on food intake. The impaired insulin sensitivity and antioxidative potency were improved and the levels of plasma glucose, total cholesterol (TC), triglycerides (TG) decreased with an increased in HDL-cholesterol (HDL-c) after NEU-P11 or melatonin administration. These data suggest that NEU-P11, like melatonin, decreased body weight gain and improved insulin sensitivity and metabolic profiles in obese rats. We conclude that NEU-P11 has a melatoninergic effect on regulating body weight in obese rats and also improving metabolic profiles and efficiently enhancing insulin sensitivity.
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PMID:NEU-P11, a novel melatonin agonist, inhibits weight gain and improves insulin sensitivity in high-fat/high-sucrose-fed rats. 1942 66

The importance of sleep to hormones and glucose metabolism was first documented more than four decades ago. Since then, sleep curtailment has become an endemic behavior in modern society. In addition, the prevalence of sleep disorders, particularly obstructive sleep apnea (OSA), has increased. OSA is very common in endocrine and metabolic disorders, but often remains undiagnosed. This Review summarizes the laboratory and epidemiologic evidence that suggests how sleep loss, either behavioral or disease-related, and poor quality of sleep might promote the development of obesity and diabetes mellitus, and exacerbate existing endocrine conditions. Treatment of sleep disorders has the potential to improve glucose metabolism and energy balance. Screening for habitual sleep patterns and OSA might be critically important for patients with endocrine and metabolic disorders.
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PMID:Effects of poor and short sleep on glucose metabolism and obesity risk. 1944 58

Recent studies have implicated the orexin system as a critical regulator of sleep/wake states as well as feeding behavior and reward processes. Orexin deficiency results in narcolepsy in humans, dogs, and rodents, suggesting that the orexin system is particularly important for maintenance of wakefulness. In addition, orexin deficiency also cause abnormalities in energy homeostasis and reward systems. Orexin activates waking active monoaminergic and cholinergic neurons in the hypothalamus and brainstem regions to maintain a long, consolidated waking period. Orexin neurons receive abundant input from the limbic system. Orexin neurons also have reciprocal links with the hypothalamic arcuate nucleus, which regulates feeding. Moreover, the responsiveness of orexin neurons to peripheral metabolic cues, such as leptin and glucose, suggest that these neurons have important role as a link between the energy homeostasis and vigilance states. Orexin neurons also have a link with the dopaminergic reward system in the ventral tegmental nucleus. These findings suggest that the orexin system interacts with systems that regulate emotion, reward, and energy homeostasis to maintain proper vigilance states. Therefore, this system may be a potentially important therapeutic target for treatment of sleep disorder, obesity, emotional stress, and addiction.
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PMID:Orexin/hypocretin: a neuropeptide at the interface of sleep, energy homeostasis, and reward system. 1954 26

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

Natural selection defined our genotype as athletes who sleep 8-9 h each night. Physical activity and sleep exhibit positive synergy, whereby each optimizes quality of and capability for the other. Our sedentary, sleep-restricted lifestyle conflicts with our genotype to generate pathophysiologic phenotypes, especially obesity. Insufficient sleep is pandemic, and other sleep disorders are increasingly common. Sleep dysfunction promotes obesity due to inactivity from sleepiness and to metabolic changes. Obesity is the primary risk factor for obstructive sleep apnea, which commonly disrupts sleep. This represents one of many pathophysiologic vicious cycles involving inactivity, sleep disorders, and obesity. Solutions include better education of the medical community, which remains surprisingly ignorant about these disease processes and therapeutic advantages of exercise and sleep repletion. Doctors commonly prescribe medications with sleep disruption or weight-gain side effects instead of lifestyle modifications. Lifestyle improvements often provide superior treatment to medications and impose no side effects.
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PMID:The role of sleep dysfunction in physical inactivity and its relationship to obesity. 1990 74

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

Sleep-disordered breathing (SDB) encompasses a group of disorders that include obstructive sleep apnoea (OSA), central sleep apnoea (CSA) and nocturnal hypoventilation. SDB commonly coexists with sleep disorders such as insomnia and restless legs syndrome, and sleep deprivation has been shown to play a role in the pathogenesis of SDB. Participants of a workshop, held at the 6th annual meeting of The International Sleep Disorders Forum: The Art of Good Sleep in 2008, evaluated whether the effective management of sleep disorders could result in a reduction in SDB. Following the workshop, a critical review of the literature in the field of sleep and SDB was conducted in order to assess the impact of improving sleep on SDB, and to determine whether measures taken to improve sleep result in a subsequent improvement in SDB. Results showed that studies evaluating the influence of improved sleep on respiratory abnormalities in patients with SDB are lacking. Studies in patients with OSA, with or without obesity-hypoventilation syndrome, show that therapy with continuous positive airways pressure and non-invasive ventilation improves sleep parameters with beneficial effects on SDB. Studies involving small numbers of patients have shown that the antidepressants fluoxetine and mirtazapine produce improvements in sleep parameters and the apnoea-hypopnoea index, and that acetazolamide may improve CSA. The benzodiazepines flurazepam, temazepam and nitrazepam, the hypnotic zolpidem, the melatonin receptor agonist ramelteon and gamma-hydroxybutyrate have all been shown to improve sleep, but are not associated with reductions or worsening in SDB. It is clear that there is a distinct knowledge gap with regard to the benefit of improving sleep disturbances for subsequent improvements in SDB. Randomized controlled clinical trials investigating the effect of pharmacological and non-pharmacological improvement of sleep disorders focusing on whether there is improvement in coexisting OSA/SDB are clearly needed. Furthermore, well-designed clinical trials investigating the role of hypnotic agents in improving SDB in certain phenotypes will enable the development of treatment recommendations for primary care physicians managing these patients in routine clinical practice.
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PMID:Can improving sleep influence sleep-disordered breathing? 2004 52


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