leptin and Sleep-Wake-Disorders

Narcolepsy, a sleep disorder characterized by loss of hypocretin neurons, has been associated with metabolic disturbances. Although the metabolic alterations in narcolepsy patients are widely investigated in the literature, the results are controversial. We performed a systematic search of literature to identify metabolic profiling studies in narcolepsy patients. A total of 48 studies were included in the meta-analysis. Narcolepsy patients exhibited higher prevalence of obesity (log OR = 0.93 [0.73-1.13], P < 0.001), diabetes mellitus (log OR = 0.64 [0.34, 0.94], P < 0.001), hypertension (log OR = 0.33 [0.11, 0.55], P < 0.001), and dyslipidemia (log OR = 1.19 [0.60, 1.77], P < 0.001) compared with non-narcoleptic controls. Narcolepsy was associated with higher BMI (SMD = 0.50 [0.32-0.68], P < 0.001), waist circumference (MD = 8.61 [2.03-15.19], P = 0.01), and plasma insulin (SMD = 0.61 [0.14-1.09], P = 0.01). Levels of fasting blood glucose (SMD = -0.25 [-0.61,0.10], P = 0.15), BMR-RMR (SMD = -0.17 [-0.52-0.18], P = 0.34), systolic blood pressure (SMD = 0.29 [-0.39-0.97], P = 0.40), diastolic blood pressure (SMD = 0.39 [-0.62, 1.40], P = 0.45), CSF melanin-concentrating hormone (MD = 5.56 [-30.79-41.91], P = 0.76), serum growth hormone (SMD = 7.84 [-7.90-23.57], P = 0.33), as well as plasma and CSF leptin (SMD = 0.10 [-1.32-1.51], P = 0.89 and MD = 0.01 [-0.02-0.04], P = 0.56, respectively) did not significantly differ between narcolepsy patients and controls. These findings necessitate early screening of metabolic alterations and cardiovascular risk factors in narcolepsy patients to reduce the morbidity and mortality rates.

Topics: Humans; Leptin; Metabolome; Narcolepsy; Obesity; Orexins; Sleep Wake Disorders

Epidemiological studies suggested an association between obesity and sleep disturbances. Obstructive sleep apnea is the most prevalent type of obesity-related sleep disorder that lead to an increased risk for numerous chronic health conditions. In addition the increased visceral adipose tissue might be responsible for the secretion of inflammatory cytokines that could contribute to alter the sleep-wake rhythm. Unhealthy food characterized by high consumption of fat and carbohydrate seems to negatively influence the quality of sleep while diet rich of fiber is associated to more restorative and deeper sleep. Although obesity could cause through several pathogenetic mechanisms an alteration of sleep, it has been reported that subjects suffering from sleep disorders are more prone to develop obesity. Experimental laboratory studies have demonstrated that decreasing either the amount or quality of sleep increase the risk of developing obesity. Experimental sleep restriction also causes physiological, hormonal and food behavioral changes that promote a positive energy balance and a compensatory disproportionate increase in food intake, decrease in physical activity, and weight gain. Thus, the aim of this review is to provide observational evidence on the association of obesity with sleep disturbances and

Topics: Diet; Endocannabinoids; Energy Metabolism; Exercise; Ghrelin; Humans; Hydrocortisone; Leptin; Melatonin; Obesity; Sleep Apnea, Obstructive; Sleep Wake Disorders; Weight Gain

Sleep is important for regulating many physiologic functions that relate to metabolism. Because of this, there is substantial evidence to suggest that sleep habits and sleep disorders are related to diabetes risk. In specific, insufficient sleep duration and/or sleep restriction in the laboratory, poor sleep quality, and sleep disorders such as insomnia and sleep apnea have all been associated with diabetes risk. This research spans epidemiologic and laboratory studies. Both physiologic mechanisms such as insulin resistance, decreased leptin, and increased ghrelin and inflammation and behavioral mechanisms such as increased food intake, impaired decision-making, and increased likelihood of other behavioral risk factors such as smoking, sedentary behavior, and alcohol use predispose to both diabetes and obesity, which itself is an important diabetes risk factor. This review describes the evidence linking sleep and diabetes risk at the population and laboratory levels.

Topics: Diabetes Mellitus; Energy Intake; Ghrelin; Humans; Insulin Resistance; Leptin; Obesity; Risk Factors; Sleep; Sleep Wake Disorders

Topics: Biomarkers; Brain; Brain-Derived Neurotrophic Factor; Child; Depressive Disorder; Ghrelin; Humans; Hypothalamo-Hypophyseal System; Inflammation; Leptin; Models, Biological; Neural Pathways; Pituitary-Adrenal System; Sleep Wake Disorders

In the last 50 years, the average self-reported sleep duration in the United States has decreased by 1.5-2 hours in parallel with an increasing prevalence of obesity and diabetes. Epidemiological studies and meta-analyses report a strong relationship between short or disturbed sleep, obesity, and abnormalities in glucose metabolism. This relationship is likely to be bidirectional and causal in nature, but many aspects remain to be elucidated. Sleep and the internal circadian clock influence a host of endocrine parameters. Sleep curtailment in humans alters multiple metabolic pathways, leading to more insulin resistance, possibly decreased energy expenditure, increased appetite, and immunological changes. On the other hand, psychological, endocrine, and anatomical abnormalities in individuals with obesity and/or diabetes can interfere with sleep duration and quality, thus creating a vicious cycle. In this review, we address mechanisms linking sleep with metabolism, highlight the need for studies conducted in real-life settings, and explore therapeutic interventions to improve sleep, with a potential beneficial effect on obesity and its comorbidities.

Topics: Adiponectin; Appetite; Diabetes Mellitus; Energy Metabolism; Female; Ghrelin; Glucose; Humans; Insulin Resistance; Leptin; Male; Melatonin; Obesity; Risk Factors; Sleep Deprivation; Sleep Wake Disorders

Classically, sleep has been considered to serve an essential restorative function for the brain. However, there are an increasing number of studies linking decreased sleep quantity and/or quality in humans to an increased obesity and diabetes risk. Reductions in sleep quantity or quality lead to an increase in hunger and appetite, which chronically could predispose an individual to obesity. Carefully controlled studies have shown that two nights of insufficient sleep is causally linked to a decrease in disposition index, the most commonly used predictor of an individual's diabetes risk, and impairments in glucose tolerance and insulin sensitivity. Thus, sleep appears to play a critical role in modulating energy metabolism in peripheral tissues. Here we will discuss recent work implicating adipose tissue as a potential direct target of disruption of sleep quality, and explore the potential mechanistic links between sleep, adipose tissue and the global control of energy metabolism in humans.

Topics: Adipocytes; Animals; Humans; Insulin Resistance; Leptin; Lipid Metabolism; Sleep; Sleep Wake Disorders; Sympathetic Nervous System

It has been long known that the frequency of overweight and obese people is higher among depressed and bipolar patients than in the general population. The marked alteration of body weight (and appetite) is one of the most frequent of the 9 symptoms of major depressive episode, and these symptoms occur during recurrent episodes of depression with a remarkably high consequence. According to studies with representative adult population samples, in case of obesity (BMI over 30) unipolar or bipolar depression is significantly more frequently (20-45%) observable. Since in case of depressed patients appetite and body weight reduction is observable during the acute phase, the more frequent obesity in case of depressed patients is related (primarily) not only to depressive episodes, but rather to lifestyle factors, to diabetes mellitus also more frequently occurring in depressed patients, to comorbid bulimia, and probably to genetic-biological factors (as well as to pharmacotherapy in case of medicated patients). At the same time, according to certain studies, circadian symptoms of depression give rise to such metabolic processes in the body which eventually lead to obesity and insulin resistance. According to studies in unipolar and bipolar patients, 57-68% of patients is overweight or obese, and the rate of metabolic syndrome was found to be between 25-49% in bipolar patients. The rate of metabolic syndrome is further increased by pharmacotherapy. Low total and HDL cholesterol level increases the risk for depression and suicide and recent studies suggest that omega-3-fatty acids possess antidepressive efficacy. Certain lifestyle factors relevant to healthy metabolism (calorie reduction in food intake, regular exercise) may be protective factors related to depression as well. The depression- and possibly suicide-provoking effect of sibutramine and rimonabant used in the pharmacotherapy of obesity is one of the greatest recent challenges for professionals and patients alike.

Topics: Anti-Obesity Agents; Antidepressive Agents; Appetite Depressants; Appetite Regulation; Bipolar Disorder; Circadian Rhythm; Cyclobutanes; Depression; Depressive Disorder, Major; Dietary Carbohydrates; Energy Intake; Ghrelin; Humans; Hypothalamo-Hypophyseal System; Insulin Resistance; Leptin; Obesity; Piperidines; Pituitary-Adrenal System; Pyrazoles; Rimonabant; Seasonal Affective Disorder; Sleep Wake Disorders; Surveys and Questionnaires; Weight Gain; Weight Loss

Recent studies reveal that sleep loss in humans leads to metabolic disorders. A new study reports the development of metabolic syndrome in mice with altered circadian timing brought about by a mutation in a gene that functions in the biological clock. An intriguing and unanswered question is the relation between a healthy biological clock and normal appetite and weight regulation.

Topics: Animals; Appetite; Circadian Rhythm; CLOCK Proteins; Feeding Behavior; Humans; Leptin; Mammals; Metabolic Syndrome; Mice; Obesity; Sleep; Sleep Wake Disorders; Trans-Activators; Weight Gain

Leptin is best known as a regulator of energy homeostasis, but it also interacts with sleep and breathing. Leptin secretion increases at night and decreases during the day. The circadian secretory profile of leptin is determined both by the hypothalamic circadian pacemaker and sleep-wake cycle. Leptin is also a powerful respiratory stimulant. Serum leptin levels are higher in obstructive sleep apnoea syndrome but lower during extended sleep deprivation in healthy subjects or in narcolepsy. Abnormalities in serum leptin concentrations have recently been linked with deleterious effects on weight control, cardiovascular health and glucose regulation. Since sleep curtailment and sleep-disordered breathing are epidemics of the modern society, better understanding of leptin pathophysiology could open new perspectives to pathophysiology of major public diseases, including obesity and metabolic syndrome.

Topics: Humans; Leptin; Receptors, Leptin; Receptors, Serotonin; Respiration; Respiration Disorders; Sleep; Sleep Wake Disorders

Sleep disorders are common in hemodialysis patients. They can affect their quality of life. The purpose of this study was to evaluate the effects of aerobic training on sleep quality, inflammatory status, and serum leptin levels in hemodialysis patients.. Twenty-eight men in the age range of 28 to 74 years who were on maintenance hemodialysis and had sleep problems were enrolled in this study. They were randomly assigned into control and training groups (14 patients in each group). Patients in the training group performed a 10- to 30-minute stationary cycling, 3 times a week, during the 1st two hours of every dialysis session, for 8 weeks. The Pittsburgh Sleep Quality Index and the Baecke questionnaire on physical activity were filled out for all participants. To assess serum leptin and C-reactive protein levels, blood samples were drawn before the beginning and at the end of the eighth week.. At the end of the study, serum leptin and C-reactive protein levels were significantly reduced (P < .001 and P < .001, respectively). Furthermore, the Pittsburgh Sleep Quality Index scores of the training group declined significantly after 8 weeks (P < .001). There was a positive correlation between sleep quality and serum levels of leptin and C-reactive protein (P = .03 and P = .04, respectively).. Aerobic exercise with moderate intensity during the first two hours of a dialysis session could improve sleep quality and inflammatory status of hemodialysis patients, which predicts morbidity, mortality, and quality of life. However, additional research is needed to confirm these effects.

Topics: Adult; Aged; C-Reactive Protein; Cross-Sectional Studies; Exercise; Humans; Leptin; Male; Middle Aged; Quality of Life; Renal Dialysis; Sleep; Sleep Wake Disorders

Short sleep appears to be strongly associated with obesity and altered metabolic function, and sleep and growth hormone (GH) secretion seems interlinked. In obesity, both the GH-insulin-like-growth-factor-I (GH-IGF-I) axis and sleep have been reported to be abnormal, however, no studies have investigated sleep in relation to the GH-IGF-I axis and weight loss in obese subjects. In this study polygraphic sleep recordings, 24-h GH release, 24-h leptin levels, free-IGF-I, total-IGF-I, IGF-binding protein-3 (IGFBP-3), acid-labile subunit (ALS), cortisol and insulin sensitivity were determined in six severely obese subjects (BMI: 41+/-1 kg/m(2), 32+/-2 years of age), cross-sectional at baseline, and longitudinal after a dramatically diet-induced weight loss (36+/-7 kg). Ten age- and gender-matched nonobese subjects served as controls. Sleep duration (360+/-17 vs. 448+/-15 min/night; P<0.01), 24-h GH (55+/-9 vs. 344+/-55 mU/l.24 h; P<0.01), free-IGF-I (2.3+/-0.42 vs. 5.7+/-1.2 microg/l; P<0.01), and total-IGF-I (186+/-21 vs. 301+/-18 microg/l; P<0.01) were significantly decreased and 24-h leptin levels were increased (35+/-5 vs. 12+/-3 microg/l; P<0.01) in obese subjects at pre-weight loss compared with nonobese subjects After diet-induced weight loss the differences in GH, free IGF-I, and leptin were no longer present between previously obese and nonobese subjects, whereas a significant difference in sleep duration and total IGF-I levels persisted. Rapid eye movement (REM) sleep, non-REM sleep, IGFBP-3, ALS, and cortisol levels were similar in obese and nonobese subjects. Sleep duration, 24-h GH, and IGF-I levels were decreased and 24-h leptin levels were increased in obese subjects. We conclude that hyposomatotropism and hyperleptinemia in obesity are transient phenomena reversible with weight loss, whereas short sleep seems to persist after weight has been reduced dramatically.

Topics: Adult; Carrier Proteins; Case-Control Studies; Circadian Rhythm; Energy Intake; Female; Glycoproteins; Human Growth Hormone; Humans; Hydrocortisone; Insulin; Insulin-Like Growth Factor Binding Protein 3; Insulin-Like Growth Factor Binding Proteins; Insulin-Like Growth Factor I; Leptin; Male; Obesity; Polysomnography; Prospective Studies; Severity of Illness Index; Sleep; Sleep Wake Disorders; Sleep, REM; Treatment Outcome; Weight Gain

Aging and menopause are associated with alterations of the sleep EEG, while age-related changes of the hypothalamo-pituitary-adrenal (HPA) axis remain controversial. Major depression is also associated with typical sleep-endocrine changes, including enhanced activity of the HPA axis, while an influence of age and gender on these alterations is less clear. To test the hypothesis that after menopause sleep-endocrine alterations associated with major depression are accentuated, we examined the sleep EEG and nocturnal hormone secretion (ACTH, cortisol, GH, estradiol, LH, FSH, and leptin) in 16 drug-free female patients, mostly with the first episode of a major depressive disorder (seven pre- and nine postmenopausal subjects) and 19 female controls (10 subjects in the early follicular phase and nine postmenopausal subjects). Nocturnal cortisol secretion was increased in postmenopausal patients with depression, while a decrease was noted in postmenopausal controls. Sleep alterations typically associated with depression, namely a reduction in sleep continuity and slow wave sleep (SWS) and an increase in REM density, were prominent in post- but not in premenopausal patients. An inverse correlation was noted between the decline in SWS and sleep continuity and FSH secretion in patients with depression, suggesting a role of menopause for these sleep-endocrine alterations typically associated with major depression. In contrast, in premenopausal patients we noted primarily a shift in SWS and delta-EEG activity from the first to the second non-REM period, which was not related to age or hormone secretion. Though the relatively small number of subjects per group precludes a definitive conclusion, our data open up the possibility that the sleep-endocrine changes typically associated with major depression are most prominent in postmenopausal patients. Whether the predominant alteration of the distribution of SWS and delta EEG activity in younger patients with a first episode of major depression has a predictive value for the future course of the disease remains to be investigated.

Topics: Adrenocorticotropic Hormone; Adult; Aged; Depressive Disorder, Major; Electroencephalography; Estradiol; Female; Follicle Stimulating Hormone; Human Growth Hormone; Humans; Hydrocortisone; Leptin; Luteinizing Hormone; Matched-Pair Analysis; Menopause; Middle Aged; Pituitary Hormones, Anterior; Polysomnography; Sleep Wake Disorders; Sleep, REM; Statistics as Topic

Topics: Adipokines; Adult; Circadian Rhythm; Female; Humans; Inflammatory Bowel Diseases; Leptin; Male; Middle Aged; Poland; Prospective Studies; Resistin; ROC Curve; Severity of Illness Index; Sleep Wake Disorders; Surveys and Questionnaires; Young Adult

We investigated relationships among immune, metabolic, and sleep abnormalities in mice with non-metastatic mammary cancer. Tumor-bearing mice displayed interleukin-6 (IL-6)-mediated peripheral inflammation, coincident with altered hepatic glucose processing and sleep. Tumor-bearing mice were hyperphagic, had reduced serum leptin concentrations, and enhanced sensitivity to exogenous ghrelin. We tested whether these phenotypes were driven by inflammation using neutralizing monoclonal antibodies against IL-6; despite the reduction in IL-6 signaling, metabolic and sleep abnormalities persisted. We next investigated neural populations coupling metabolism and sleep, and observed altered activity within lateral-hypothalamic hypocretin/orexin (HO) neurons. We used a dual HO-receptor antagonist to test whether increased HO signaling was causing metabolic abnormalities. This approach rescued metabolic abnormalities and enhanced sleep quality in tumor-bearing mice. Peripheral sympathetic denervation prevented tumor-induced increases in serum glucose. Our results link metabolic and sleep abnormalities via the HO system, and provide evidence that central neuromodulators contribute to tumor-induced changes in metabolism.

Topics: Animals; Breast Neoplasms; Cell Line, Tumor; Female; Ghrelin; Glucose; Hyperphagia; Interleukin-6; Leptin; Mammary Neoplasms, Experimental; Metabolic Diseases; Mice; Mice, Inbred BALB C; Neurons; Orexin Receptor Antagonists; Orexins; Sleep; Sleep Wake Disorders

This pilot study examined associations between sleep quality and metabolic risk profiles, underlying hormones, inflammatory markers, and behaviors in overweight and obese young adults, aged 18-29 years.. Cross-sectional, descriptive, correlational study design.. A partial sample ( n = 29) was re-recruited from a parent study on screening for risk of early-onset diabetes. BodyMedia's SenseWear® armband was used to assess sleep quality. Based on the percentage of consolidated sleep days during the past week, participants were classified as poor, fair, or good sleepers. Multiple multivariate general linear models were used to examine group differences in study variables after adjusting for obesity impact.. There were no significant differences among groups in age (mean 23.5 ± 2.9 years) or body mass index (mean 38.0 ± 8.9 kg/m. Overweight/obese young adults had irregular sleep schedules and patterns, indicators of poor sleep quality, that were possibly associated with changes in dietary behaviors and underlying plasma hormones. In addition to traditional clinical cardiometabolic markers, plasma resistin and ghrelin may be good predictors of heightened vulnerability to cardiometabolic diseases in overweight/obese young adults with poor-quality sleep.

Topics: Adiponectin; Adolescent; Adult; Biomarkers; Body Mass Index; Cross-Sectional Studies; Feeding Behavior; Female; Healthy Volunteers; Humans; Leptin; Male; Obesity; Overweight; Pilot Projects; Sleep Wake Disorders; Young Adult

Sleep duration is associated with adiposity in adults. Abdominal adiposity specifically is strongly correlated with metabolic alterations, however, the relationships between abdominal adiposity and sleep quality are incompletely understood. The purpose of this study is to test the hypothesis that abdominal adiposity is related to poor sleep quality while total adiposity is not; and to explore whether pathways, including immune system and hypothalamic-pituitary-adrenal axis, link abdominal adiposity to poor sleep quality.. Subjects were 101 men and women aged 38.88 ± 11.96 years with body mass index between 29.35 ± 6.93 kg/m. Poor sleep quality was related to greater visceral fat (r = 0.26; p < 0.05), but not total fat. The PSQ group had greater visceral fat compared to the NSQ group (1.11 ± 0.83 kg vs 0.79 ± 0.62 kg; p < 0.05), however, there was no difference in total fat mass (33.18 ± 14.21 kg vs 29.39 ± 13.03 kg; p = 0.24). The PSQ group had significantly greater leptin (1.37 ± 0.07 ng/ml vs 1.08 ± 0.08 ng/ml; p < 0.05), but hypothalamic-pituitary-adrenal axis activity did not differ between the PSQ and NSQ groups.. Poor sleep quality is associated with greater visceral adiposity and leptin secretion. Further research is needed to probe potential cause and effect relationships among visceral adipose tissue, leptin, and sleep quality.

Topics: Abdominal Fat; Adiposity; Adult; Body Composition; Body Mass Index; Cross-Sectional Studies; Female; Humans; Hypothalamo-Hypophyseal System; Intra-Abdominal Fat; Leptin; Male; Middle Aged; Obesity; Obesity, Abdominal; Pituitary-Adrenal System; Sleep; Sleep Wake Disorders

Leptin, a pleiotropic protein hormone produced mainly by fat cells, regulates metabolic activity and many other physiological functions. The intrinsic circadian rhythm of blood leptin is modulated by gender, development, feeding, fasting, sleep, obesity, and endocrine disorders. Hyperleptinemia is implicated in leptin resistance. To determine the specificity and sensitivity of leptin concentrations in sleep disorders, we summarize here the alterations of leptin in four conditions in animal and human studies: short duration of sleep, sleep fragmentation, obstructive sleep apnea (OSA), and after use of continuous positive airway pressure (CPAP) to treat OSA. The presence and causes of contradictory findings are discussed. Though sustained insufficient sleep lowers fasting blood leptin and therefore probably contributes to increased appetite, obesity and OSA independently result in hyperleptinemia. Successful treatment of OSA by CPAP is predicted to decrease hyperleptinemia, making leptin an ancillary biomarker for treatment efficacy. Current controversies also call for translational studies to determine how sleep disorders regulate leptin homeostasis and how the information can be used to improve sleep treatment.

Topics: Appetite; Biomarkers; Continuous Positive Airway Pressure; Humans; Leptin; Obesity; Sleep Apnea, Obstructive; Sleep Deprivation; Sleep Wake Disorders; Treatment Outcome

Higher plasma levels of leptin have been associated with increased cardiometabolic risk. The aim of this study was to investigate the association between short duration of sleep and hyperleptinemia in Taiwanese adults.. We examined the association between duration of sleep and hyperleptinemia in 254 men and women recruited from the physical examination center at a regional hospital in southern Taiwan. Hyperleptinemia was defined as a plasma leptin level of 8.13 ng/mL and above. Short sleep duration was defined as < 6.5 h/day. Multiple logistic regression analysis was used to assess the association between short duration of sleep and hyperleptinemia.. In females, short duration of sleep (< 6.5 h/day; OR = 2.15, 95% CI = 0.99-4.78), greater hip circumference (OR = 3.00, CI = 1.13-8.78), higher percent body fat (OR = 1.75, CI = 1.07-2.95), and higher white blood cell counts (OR = 1.67, CI = 1.26-2.28) were associated with an increased risk of hyperleptinemia. In males, greater body weight was significantly associated with an increased risk of hyperleptinemia (OR = 3.55, 95% CI = 1.46-10.23). There was also a trend of association (p = 0.096) between short duration of sleep and an increased risk of hyperleptinemia (OR = 4.98, 95% CI = 0.80-42.40).. In this study of healthy Taiwanese adults, short duration of sleep was significantly associated with hyperleptinemia in women, and the association was independent of adiposity.

Topics: Adipose Tissue; Adult; Age Factors; Anthropometry; Body Mass Index; Cohort Studies; Comorbidity; Confidence Intervals; Female; Healthy Volunteers; Humans; Leptin; Logistic Models; Male; Middle Aged; Multivariate Analysis; Obesity; Odds Ratio; Risk Assessment; Sex Factors; Sleep; Sleep Wake Disorders; Young Adult

Leptin, involved in energy regulation and contributor to cardiovascular disease, has been implicated to play a role in depression and sleep disturbances, two closely intertwined conditions. Previous results investigating leptin level alterations either in sleep disorders or in depression have been inconsistent. We investigate the association between leptin levels and the different combinations of depressed mood and sleep disturbances in 1369 subjects (706 men, 663 women), derived from the population-based MONIKA/KORA study. As leptin regulation is known to differ by sex and weight, analyses were performed in normal weight and overweight men and women separately. We found a highly significant association between leptin levels and the combination of depressed mood and sleep disturbances in normal-weight women (BMI ≤ 25) (p<0.01). No associations were found in men and in overweight women. Our results suggest that leptin regulation in depressed mood and sleep disturbances very much depend on sex and weight.

Topics: Adult; Aged; Analysis of Variance; Association; C-Reactive Protein; Chi-Square Distribution; Cholesterol; Cholesterol, HDL; Cohort Studies; Community Health Planning; Depressive Disorder; Female; Humans; Immunoradiometric Assay; Leptin; Male; Middle Aged; Obesity; Psychometrics; Retrospective Studies; Risk Factors; Sleep Wake Disorders; Surveys and Questionnaires

The obesity pandemic is claiming its presence even among youngest of children and is clearly on the rise. Although the extent and implications of this massive increase in the prevalence of overweight and obese children are unclear, they are anticipated to be deleterious to global health outcomes and life expectancy. The potential interrelationships between sleep and obesity have gained recent attention. In this chapter, we initially examine the critical evidence supporting or refuting such proposed associations. In addition, the potential reciprocal roles of obesity and obstructive sleep apnea in the facilitation of their pathophysiology are also reviewed, along with their amplificatory effects on their respective morbidities.

Topics: Adolescent; Airway Resistance; Child; Comorbidity; Humans; Leptin; Obesity; Prevalence; Sleep Apnea, Obstructive; Sleep Wake Disorders

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.

Topics: Cytokines; Diabetes Mellitus, Type 2; Ghrelin; Humans; Inflammation; Leptin; Obesity; Restless Legs Syndrome; Sleep Wake Disorders

The purpose of this work was to determine whether, in children with metabolic syndrome and sleep-disordered breathing, metabolic markers separate them from children with metabolic syndrome without sleep-disordered breathing and whether treatment of sleep-disordered breathing with continuous positive airway pressure is associated with an improvement in metabolic derangement.. Subjects aged 7 to 19 years old with metabolic syndrome and a positive validated sleep questionnaire were recruited. Subjects underwent overnight polysomnography, during which sympathetic nervous system activity was assessed via 8-hourly measurements of norepinephrine and epinephrine, together with leptin. The next morning, a fasting 3-hour oral glucose-tolerance test was performed to calculate whole-body insulin sensitivity. A fasting lipid panel interleukin 6, adiponectin, and C-reactive protein levels were also measured. Children with sleep-disordered breathing were placed on continuous positive airway pressure for 3 months and studied again. Sleep-disordered breathing and no sleep-disordered breathing groups were compared by using Fisher's exact test and t test for independent samples with analysis of covariance to adjust for age and BMI.. Of 34 children studied, 25 had sleep-disordered breathing (apnea-hypopnea index: >1.5). Mean hourly norepinephrine and leptin levels were higher in the group with sleep-disordered breathing compared with the group without sleep-disordered breathing (P < .005), with no difference in whole-body insulin sensitivity. Eleven subjects with sleep-disordered breathing completed 3 months of nightly continuous positive airway pressure treatment. In the follow-up study, mean hourly leptin levels were significantly lower than in the initial study, with no change in BMI z score or other measurements.. Our findings support the hypothesis that sleep-disordered breathing in children with metabolic syndrome is associated with increased sympathetic nervous system activity and leptin levels but not worsening of insulin resistance. Treatment of sleep-disordered breathing with continuous positive airway pressure led to a significant decrease in leptin levels.

Topics: Adolescent; Biomarkers; Child; Continuous Positive Airway Pressure; Enzyme-Linked Immunosorbent Assay; Female; Follow-Up Studies; Humans; Leptin; Male; Metabolic Syndrome; Polysomnography; Respiration; Sleep Wake Disorders; Treatment Outcome

To determine if hypocretin deficiency is associated with abnormally low serum leptin levels, a putative cause of increased body mass index in narcoleptics.. Cross-sectional controlled study.. Three hundred seventy subjects, including 111 healthy controls, 93 narcoleptic subjects with hypocretin deficiency (cerebrospinal fluid [CSF] hypocretin-1 levels < 110 pg/mL), 72 narcoleptic subjects with normal hypocretin levels, and 89 subjects with other sleep disorders. After completing the Stanford Sleepiness Inventory, participants underwent spinal taps and blood sampling for measurement of CSF leptin and hypocretin-1 levels, HLA DQB1*0602 phenotyping, and serum leptin and C-reactive protein levels.. Serum leptin levels were similar in narcoleptic subjects, whether hypocretin-deficient (13.2 +/- 1.7 ng/mL, mean +/- SEM) or not (13.0 +/- 1.8 ng/mL), controls (10.1 +/- 1.1 ng/mL) and subjects with other sleep disorders (11.5 +/- 1.6 ng/mL). Similarly, the CSF leptin levels and the CSF: serum leptin ratios (an indicator of brain leptin uptake) were not different between groups. Serum and CSF leptin levels were higher in women and in subjects with higher body mass indexes. Leptin brain uptake decreased in women, in the aged, and in more-obese subjects. In contrast with a presumed inhibitory effect of leptin on hypocretin-containing cells, CSF leptin levels tended to correlate positively with CSF hypocretin-1 levels. C-reactive protein was higher (4.2 +/- 0.9 mg/L) in narcoleptic subjects with hypocretin deficiency than in controls (1.4 +/- 0.3 mg/L, p = .0055), a difference still significant after adjustment on confounding factors.. Our data do not support a role for leptin in mediating increased body mass index in narcolepsy. A moderate but selective increase in C-reactive protein in hypocretin-1 deficient subjects should prompt research on inflammation in narcolepsy.

Topics: Adult; Blood-Brain Barrier; Body Mass Index; Brain; C-Reactive Protein; Cross-Sectional Studies; Female; HLA-DQ Antigens; HLA-DQ beta-Chains; Humans; Leptin; Male; Middle Aged; Narcolepsy; Obesity; Orexin Receptors; Phenotype; Receptors, G-Protein-Coupled; Receptors, Leptin; Receptors, Neuropeptide; Reference Values; Sex Factors; Sleep Wake Disorders

To compare the characteristics of obese persons with the night eating syndrome (NES) with those of nonobese persons with the NES.. Eighty subjects (40 with a body mass index [BMI] greater than 30 and 40 with a BMI less than 25) identified themselves on a website for the Night Eating Questionnaire (NEQ) as suffering from the NES. The responses of the 40 obese website subjects were compared with 21 obese persons with the NES who had undergone face-to-face interviews. The responses on the NEQ of the 40 obese and the 40 non-obese website subjects were then compared.. There was no difference in the NEQ results of the 40 website obese subjects and 21 obese night eaters who had undergone face-to-face interviews. The responses of these same 40 obese subjects showed very little difference compared with those of the 40 nonobese subjects. The major difference between the two groups was the considerable younger age of the normal-weight NES subjects.. The striking similarity in the characteristics between obese and nonobese subjects with the NES indicates that this disorder, considered until now to occur primarily among obese persons, also occurs among nonobese persons. The younger age of the nonobese subjects suggests that the NES may contribute to the development of obesity.

Topics: Adult; Body Mass Index; Circadian Rhythm; Feeding and Eating Disorders; Female; Humans; Leptin; Obesity; Sleep Wake Disorders; Surveys and Questionnaires

Sleep duration may be an important regulator of body weight and metabolism. An association between short habitual sleep time and increased body mass index (BMI) has been reported in large population samples. The potential role of metabolic hormones in this association is unknown.. Study participants were 1,024 volunteers from the Wisconsin Sleep Cohort Study, a population-based longitudinal study of sleep disorders. Participants underwent nocturnal polysomnography and reported on their sleep habits through questionnaires and sleep diaries. Following polysomnography, morning, fasted blood samples were evaluated for serum leptin and ghrelin (two key opposing hormones in appetite regulation), adiponectin, insulin, glucose, and lipid profile. Relationships among these measures, BMI, and sleep duration (habitual and immediately prior to blood sampling) were examined using multiple variable regressions with control for confounding factors. A U-shaped curvilinear association between sleep duration and BMI was observed. In persons sleeping less than 8 h (74.4% of the sample), increased BMI was proportional to decreased sleep. Short sleep was associated with low leptin (p for slope = 0.01), with a predicted 15.5% lower leptin for habitual sleep of 5 h versus 8 h, and high ghrelin (p for slope = 0.008), with a predicted 14.9% higher ghrelin for nocturnal (polysomnographic) sleep of 5 h versus 8 h, independent of BMI.. Participants with short sleep had reduced leptin and elevated ghrelin. These differences in leptin and ghrelin are likely to increase appetite, possibly explaining the increased BMI observed with short sleep duration. In Western societies, where chronic sleep restriction is common and food is widely available, changes in appetite regulatory hormones with sleep curtailment may contribute to obesity.

Topics: Adult; Appetite; Body Mass Index; Body Weight; Female; Ghrelin; Humans; Leptin; Longitudinal Studies; Male; Middle Aged; Obesity; Peptide Hormones; Sleep; Sleep Wake Disorders