leptin and Sleep-Apnea-Syndromes

The availability of high-quality studies on the association between sleep-disordered breathing in children and delayed growth associated with the hormonal profile recorded before surgery and at follow-up is limited.. Medline PubMed, Scopus and WebOfScience databases were searched for relevant publications published between January 2008 to January 2020 and a total of 261 potentially eligible studies were identified.. Following review 19 papers were eligible for inclusion: seven reported a significant postsurgical increase in growth regardless of initial weight status, type of surgery, type of study design, and length of follow-up period. The only high-quality study was a randomized controlled trial that found an increased risk of obstructive sleep apnea syndrome relapse in overweight children. Twelve studies reported the significant increase in growth parameters showing that IGF-1, IGFBP-3, and ghrelin may boost growth after surgery.. The current systematic review demonstrates a scarcity of high-quality studies on growth delay in children with sleep-disordered breathing. Significant catch-up growth after surgery in the short term and changes in IGF-1, IGFBP-3, ghrelin, and leptin levels has been reported in most published studies.

Topics: Adenoidectomy; Adolescent; Adolescent Development; Age Factors; Biomarkers; Child; Child Development; Child, Preschool; Ghrelin; Growth Disorders; Humans; Infant; Insulin-Like Growth Factor Binding Protein 3; Insulin-Like Growth Factor I; Leptin; Risk Assessment; Risk Factors; Sleep Apnea Syndromes; Tonsillectomy; Treatment Outcome

Obesity is a global epidemic in developed countries accounting for many of the metabolic and cardiorespiratory morbidities that occur in adults. These morbidities include type 2 diabetes, sleep-disordered breathing (SDB), obstructive sleep apnea, chronic intermittent hypoxia, and hypertension. Leptin, produced by adipocytes, is a master regulator of metabolism and of many other biological functions including central and peripheral circuits that control breathing. By binding to receptors on cells and neurons in the brainstem, hypothalamus, and carotid body, leptin links energy and metabolism to breathing. In this comprehensive article, we review the central and peripheral locations of leptin's actions that affect cardiorespiratory responses during health and disease, with a particular focus on obesity, SDB, and its effects during early development. Obesity-induced hyperleptinemia is associated with centrally mediated hypoventilation with decrease CO

Topics: Adiponectin; Animals; Humans; Leptin; Metabolism, Inborn Errors; Obesity; Sleep Apnea Syndromes; Sleep Apnea, Obstructive

Despite the early recognition of the strong association between obstructive sleep apnoea (OSA) and obesity, and OSA and cardiovascular problems, sleep apnoea has been treated as a "local abnormality" of the respiratory track rather than as a "systemic illness". In 1997, we first reported that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNFalpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. In subsequent studies, it was shown that IL-6, TNFalpha, and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat was the primary parameter linked with sleep apnoea. Further studies showed that women with the polycystic ovary syndrome (PCOS) were much more likely than controls to have sleep-disordered breathing (SDB) and daytime sleepiness, suggesting a pathogenetic role of insulin resistance in OSA. Additional accumulated evidence that supports the role of obesity and the associated metabolic aberrations in the pathogenesis of sleep apnoea and related symptoms include: obesity without sleep apnoea is associated with daytime sleepiness; the protective role of gonadal hormones as suggested by the increased prevalence of sleep apnoea in post-menopausal women and the significantly reduced risk for OSA in women on hormonal therapy; partial effects of continuous positive airway pressure (CPAP) in obese patients with apnoea on hypercytokinemia, insulin resistance indices, and visceral fat; and that the prevalence of the metabolic syndrome in the U.S. population from the Third National Health and Nutrition Examination Survey (1988-1994) parallels the prevalence of symptomatic sleep apnoea in general random samples. Furthermore, the beneficial effect of a cytokine antagonist on EDS and apnoea in obese, male apnoeics and that of exercise and weight loss on SDB and EDS in general random or clinical samples, supports the hypothesis that cytokines and insulin resistance are mediators of EDS and sleep apnoea in humans. Finally, our recent finding that in obese, hypothalamic CRH neuron is hypoactive, provides additional evidence on the potential central neural mechanisms for depressed ventilation and consequent development of sleep apnoea in obese individuals. In conclusion, accumulating evidence provides support to our thesis that obesity via inflammation, insulin resistance, visceral adiposity, and

Topics: Adiposity; Female; Humans; Inflammation; Insulin Resistance; Intra-Abdominal Fat; Leptin; Male; Metabolic Syndrome; Models, Biological; Obesity; Polycystic Ovary Syndrome; Sleep Apnea Syndromes

Obesity is associated with significant morbidity and mortality and is increasing in prevalence worldwide. Associated conditions include insulin resistance (IR), diabetes, hypertension and dyslipidaemia; a clustering of these has recently been termed as metabolic syndrome. Weight gain is a major predictor of the metabolic syndrome with waist circumference being a more sensitive indicator than body mass index as it reflects both abdominal subcutaneous adipose tissue and visceral adipose tissue (VAT). VAT has more metabolic activity and secretes a number of hormones and pro-inflammatory cytokines which are linked with the metabolic abnormalities listed above. Central obesity also increases the risk of obstructive sleep apnoea syndrome (OSAS), where the sleep disordered breathing may also independently lead to/or exacerbate IR, diabetes and cardiovascular risk. The contribution of OSAS to the metabolic syndrome has been under-recognized. The putative mechanisms by which OSAS causes or exacerbates these other abnormalities are discussed. We propose that activation of nuclear factor kappa B by stress hypoxia and/or by increased adipokines and free fatty acids released by excess adipose tissue is the final common inflammatory pathway linking obesity, OSAS and the metabolic syndrome both individually and, in many cases, synergistically.

Topics: Adiponectin; Diabetes Mellitus, Type 2; Humans; Inflammation; Insulin Resistance; Leptin; Metabolic Syndrome; NF-kappa B; Obesity; Risk Factors; Sleep Apnea Syndromes

Topics: Apolipoproteins E; Genetic Predisposition to Disease; Genotype; Humans; Leptin; Obesity; Phenotype; Sleep Apnea Syndromes

The obesity epidemic is driving metabolic (insulin resistance) syndrome-related health problems including an approximately threefold increased coronary heart disease risk. Sympathetic hyperfunction may participate in the pathogenesis and complications of the metabolic syndrome including higher blood pressure, a more active renin-angiotensin system, insulin resistance, faster heart rates, and excess cardiovascular disease including sudden death. Possible factors augmenting sympathetic activation in the metabolic syndrome include alterations of insulin, leptin, nonesterified fatty acids (NEFAs), cytokines, tri-iodothyronine, eicosanoids, sleep apnea, nitric oxide, endorphins, and neuropeptide Y. Of note, high plasma NEFAs are a risk factor for hypertension and sudden death. In short-term human studies, NEFAs can raise blood pressure, heart rate, and a(1)-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance. Efforts to further identify the mechanisms and consequences of sympathetic dysfunction in the metabolic syndrome may provide insights for therapeutic advances to ameliorate the excess cardiovascular risk and adverse outcomes.

Topics: Cardiovascular Diseases; Fatty Acids, Nonesterified; Humans; Hypertension; Insulin Resistance; Leptin; Metabolic Syndrome; Muscle, Skeletal; Obesity; Risk Factors; Sleep Apnea Syndromes; Sympathetic Nervous System

Patients with sleep disordered breathing (SDB) are at increased risk for cardiovascular disease including hypertension, angina, myocardial infarction, and stroke. Neurohumoral and hemodynamic responses to untreated sleep apnea are likely mechanisms that produce functional and structural changes within the cardiovascular system. Obesity, higher blood pressure, and advancing age, which are common characteristics of patients with SDB, contribute to the overall risk for cardiovascular disease. Recent studies indicate that OSA is associated with or aggravates other risk markers for cardiovascular disease. These factors include leptin, C-reactive protein, homocysteine, and insulin resistance syndrome. Elevations in C-reactive protein and glucose intolerance may be correlated with the severity of SDB. The impact of alleviating SDB on these cardiovascular risk factors has not been fully elucidated. Regardless, assessment of overall cardiovascular risk in patients with sleep apnea is warranted to identify those individuals that are high-risk who require immediate attention and intervention or in those that should be treated more aggressively.

Topics: Biomarkers; C-Reactive Protein; Cardiovascular Diseases; Homocysteine; Humans; Leptin; Metabolic Syndrome; Positive-Pressure Respiration; Risk Factors; Severity of Illness Index; Sleep Apnea Syndromes

There are several mechanisms by which pharmacologic agents might improve sleep related breathing disorders. Upper airway muscle atony during sleep and fat deposition on the upper airway walls are critical in the pathogenesis of upper airway obstruction. As central neuromediators that regulate upper airway muscle activity, serotonin, gamma amino-butyric acid and thyrotropin releasing hormone are reviewed. Although agonists or antagonists of these mediators changed the upper airway muscle activity, no agents have successfully improved sleep related breathing disorders. Leptin is a protein produced by adipose tissue that interacts with receptors in the hypothalamus to inhibit eating. Leptin might have therapeutic potential for obesity-related breathing disorders related to a relative deficiency in leptin, or a leptin resistance.

Topics: Airway Obstruction; GABA Antagonists; gamma-Aminobutyric Acid; Humans; Leptin; Serotonin; Serotonin Receptor Agonists; Sleep Apnea Syndromes; Thyrotropin-Releasing Hormone

Sleep apnea and associated daytime sleepiness and fatigue are common manifestations of mainly obese middle-aged men. The onset of sleep apnea peaks in middle age, and its morbid and mortal sequelae include complications from accidents and cardiovascular events. The pathophysiology of sleep apnea remains obscure. The purpose of this study was to test three separate, albeit closely related, hypotheses. 1) Does sleep apnea contribute to the previously reported changes of plasma cytokine (tumor necrosis factor-alpha and interleukin-6) and leptin levels independently of obesity? 2) Among obese patients, is it generalized or visceral obesity that predisposes to sleep apnea? 3) Is apnea a factor independent from obesity in the development of insulin resistance? Obese middle-aged men with sleep apnea were first compared with nonapneic age- and body mass index (BMI)-matched obese and age-matched lean men. All subjects were monitored in the sleep laboratory for 4 consecutive nights. We obtained simultaneous indexes of sleep, sleep stages, and sleep apnea, including apnea/hypopnea index and percent minimum oxygen saturation. The sleep apneic men had higher plasma concentrations of the adipose tissue-derived hormone, leptin, and of the inflammatory, fatigue-causing, and insulin resistance-producing cytokines tumor necrosis factor-alpha and interleukin-6 than nonapneic obese men, who had intermediate values, or lean men, who had the lowest values. Because these findings suggested that sleep apneics might have a higher degree of insulin resistance than the BMI-matched controls, we studied groups of sleep-apneic obese and age- and BMI-matched nonapneic controls in whom we obtained computed tomographic scan measures of total, sc, and visceral abdominal fat, and additional biochemical indexes of insulin resistance, including fasting plasma glucose and insulin. The sleep apnea patients had a significantly greater amount of visceral fat compared to obese controls (<0.05) and indexes of sleep disordered breathing were positively correlated with visceral fat, but not with BMI or total or sc fat. Furthermore, the biochemical data confirmed a higher degree of insulin resistance in the group of apneics than in BMI-matched nonapneic controls. We conclude that there is a strong independent association among sleep apnea, visceral obesity, insulin resistance and hypercytokinemia, which may contribute to the pathological manifestations and somatic sequelae of this condition.

Topics: Analysis of Variance; Blood Pressure; Body Composition; Cytokines; Fatigue; Humans; Insulin Resistance; Interleukin-6; Leptin; Male; Middle Aged; Obesity; Respiratory Mechanics; Sleep Apnea Syndromes; Sleep Stages; Tomography, X-Ray Computed; Tumor Necrosis Factor-alpha

Topics: Adult; Humans; Insulin Resistance; Leptin; Middle Aged; Positive-Pressure Respiration; Proteins; Sleep Apnea Syndromes

Leptin, a hormone related to satiety, has been studied because of its association with obesity and sleep apnea. The distribution of leptin receptors in the brain stem, and in the hypoglossal nucleus, has not yet been described. The stimulation of these muscles has been studied in the treatment of sleep apnea.. to detail the presence of leptin receptors in the nuclei of these nerves to enable studies of stimulation of this region through leptin.. the brains of five cadavers, removed during necropsy, collected at the Death Verification Service were included. An informed consent was signed by a family member (wife, mother or son/daughter) who answered specific questionnaire concerning comorbities. Anthropometric measurements were recorded. The medulla oblongata and pons fragments were identified. Immunohistochemical staining analysis was performed to identify the location of the leptin receptors.. In the immunohistochemical analysis an intense staining signal of the brownish coloration of neurons was evidenced in the hypoglossal nerve nucleus, moderate in the olivary nucleus and mild in the dorsal nucleus of the vagus and trigeminal nucleus. In motor neurons, more intense brown pigmentation can be observed in the nucleus and cytoplasm when compared to sensory neurons.. The immunoexpression of leptin receptor was demonstrated in the motor neurons of the human hypoglossal nucleus. These results may contribute to unravel details of the pathophysiology of neuromuscular control of airway collapse during sleep and to the development of new drugs capable of improving the neuromuscular tone of upper airway in apneic individuals.

Topics: Airway Resistance; Brain Stem; Humans; Leptin; Motor Neurons; Receptors, Leptin; Sleep; Sleep Apnea Syndromes

Sleep-disordered breathing (SDB) affects over 50% of obese individuals. Exaggerated hypoxic chemoreflex is a cardinal trait of SDB in obesity. We have shown that leptin acts in the carotid bodies (CB) to augment chemoreflex and that leptin activates the transient receptor potential melastatin 7 (TRPM7) channel. However, the effect of leptin-TRPM7 signalling in CB on breathing and SDB has not been characterized in diet-induced obesity (DIO). We hypothesized that leptin acts via TRPM7 in the CB to increase chemoreflex leading to SDB in obesity. DIO mice were implanted with EEG/EMG electrodes and transfected with Lepr

Topics: Animals; Carotid Body; Hypoventilation; Hypoxia; Leptin; Mice; Mice, Obese; Obesity; RNA, Small Interfering; Sleep; Sleep Apnea Syndromes; Transient Receptor Potential Channels; TRPM Cation Channels

Topics: Animals; Extracellular Vesicles; Leptin; Mice; Obesity; Sleep Apnea Syndromes

Obstructive sleep apnea (OSA) is recurrent obstruction of the upper airway due to the loss of upper airway muscle tone during sleep. OSA is highly prevalent, especially in obesity. There is no pharmacotherapy for OSA. Previous studies have demonstrated the role of leptin, an adipose-tissue-produced hormone, as a potent respiratory stimulant. Leptin signaling via a long functional isoform of leptin receptor, LEPR

Topics: Animals; Electromyography; Leptin; Male; Mice, Inbred C57BL; Mice, Transgenic; Neurons; Obesity; Receptors, Drug; Receptors, Leptin; Sleep Apnea Syndromes; Sleep, REM; Solitary Nucleus

Respiratory depression is the main cause of morbidity and mortality associated with opioids. Obesity increases opioid-related mortality, which is mostly related to comorbid obstructive sleep apnea. Naloxone, a μ-opioid receptor blocker, is an effective antidote, but it reverses analgesia. Like humans with obesity, mice with diet-induced obesity hypoventilate during sleep and develop obstructive sleep apnea, which can be treated with intranasal leptin. We hypothesized that intranasal leptin reverses opioid-induced sleep-disordered breathing in obese mice without decreasing analgesia. To test this hypothesis, mice with diet-induced obesity were treated with morphine at 10 mg/kg subcutaneously and with leptin or placebo intranasally. Sleep and breathing were recorded by barometric plethysmography, and pain sensitivity was measured by the tail-flick test. Excitatory postsynaptic currents were recorded

Topics: Administration, Intranasal; Analgesia; Analgesics, Opioid; Animals; Disease Models, Animal; Enkephalins; Excitatory Postsynaptic Potentials; Leptin; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Morphine; Motor Neurons; Receptors, Opioid, mu; Respiration; Sleep; Sleep Apnea Syndromes; Synaptic Transmission

Topics: Administration, Intranasal; Animals; Leptin; Mice; Mice, Obese; Sleep Apnea Syndromes

Leptin treats upper airway obstruction and alveolar hypoventilation in leptin-deficient ob/ob mice. However, obese humans and mice with diet-induced obesity (DIO) are resistant to leptin because of poor permeability of the blood-brain barrier. We propose that intranasal leptin will bypass leptin resistance and treat sleep-disordered breathing in obesity.. To assess if intranasal leptin can treat obesity hypoventilation and upper airway obstruction during sleep in mice with DIO.. Male C57BL/6J mice were fed with a high-fat diet for 16 weeks. A single dose of leptin (0.4 mg/kg) or BSA (vehicle) were administered intranasally or intraperitoneally, followed by either sleep studies (n = 10) or energy expenditure measurements (n = 10). A subset of mice was treated with leptin daily for 14 days for metabolic outcomes (n = 20). In a separate experiment, retrograde viral tracers were used to examine connections between leptin receptors and respiratory motoneurons.. Acute intranasal, but not intraperitoneal, leptin decreased the number of oxygen desaturation events in REM sleep, and increased ventilation in non-REM and REM sleep, independently of metabolic effects. Chronic intranasal leptin decreased food intake and body weight, whereas intraperitoneal leptin had no effect. Intranasal leptin induced signal transducer and activator of transcription 3 phosphorylation in hypothalamic and medullary centers, whereas intraperitoneal leptin had no effect. Leptin receptor-positive cells were synaptically connected to respiratory motoneurons.. In mice with DIO, intranasal leptin bypassed leptin resistance and significantly attenuated sleep-disordered breathing independently of body weight.

Topics: Animals; Humans; Leptin; Mice; Mice, Inbred C57BL; Models, Animal; Nasal Absorption; Obesity; Sleep; Sleep Apnea Syndromes

Topics: Animals; Diet; Leptin; Mice; Obesity; Receptors, Leptin; Sleep Apnea Syndromes

Deoxyribonucleic acid (DNA) methylation is an epigenetic modification involved in gene expression regulation, usually via gene silencing, which contributes to the risks of many multifactorial diseases. The aim of the present study was to analyze the influence of resting oxygen consumption on global and gene DNA methylation as well as protein secretion of inflammatory markers in blood cells from obese subjects with sleep apnea-hypopnea syndrome (SAHS).. A total of 44 obese participants with SAHS were categorized in 2 groups according to their resting oxygen consumption. DNA methylation levels were evaluated using a methylation-sensitive high resolution melting approach.. The analyzed interleukin 6 (IL6) gene cytosine phosphate guanine (CpG) islands showed a hypomethylation, while serum IL-6 was higher in the low compared to the high oxygen consumption group (p < 0.05). Moreover, an age-related loss of DNA methylation of tumor necrosis factor (B = -0.82, 95% CI -1.33 to -0.30) and long interspersed nucleotide element 1 (B = -0.46; 95% CI -0.87 to -0.04) gene CpGs were found. Finally, studied CpG methylation levels of serpin peptidase inhibitor, clade E member 1 (r = 0.43; p = 0.01), and IL6 (r = 0.41; p = 0.02) were positively associated with fat-free mass.. These findings suggest a potential role of oxygen in the regulation of inflammatory genes. Oxygen consumption measurement at rest could be proposed as a clinical biomarker of metabolic health.

Topics: Adiponectin; Adult; Biomarkers; Body Mass Index; C-Reactive Protein; CpG Islands; DNA Methylation; Epigenesis, Genetic; Gene Expression Regulation; Hemodynamics; Humans; Interleukin-6; Leptin; Long Interspersed Nucleotide Elements; Male; Middle Aged; Obesity; Oxygen Consumption; Plasminogen Activator Inhibitor 1; Promoter Regions, Genetic; Serpins; Sleep Apnea Syndromes; Tumor Necrosis Factor-alpha

Obesity is an important risk factor for sleep disorders. This study aimed to evaluate the association of leptin, zinc and tryptophan (TRP) in obese subjects with sleep deficits [sleep apnea (SA), insomnia (IN)]. In this cross sectional case control, with the verbal and written consent 206, obese with sleep deficits and 30, non-obese/normal identified from various areas of Karachi, Pakistan. The socio-demographic data including; age, body mass index (BMI), education and residence, of participants was collected. After providing informed consent, fasting blood samples were taken and serum was collected. The serum concentration of leptin, zinc and TRP were analyzed by ELISA (Enzyme-linked immunosorbent assay), FAAS (Flame atomic absorption spectrophotometer) and HPLC (High performance liquid chromatography) respectively. A significant correlation was found between BMI (body mass index) and leptin, BMI and zinc, BMI and TRP. The correlation between leptin consecutively was significantly associated with zinc and TRP in obese patients. Sleep deficits elevated circulatory levels of leptin while lower zinc and TRP levels compared to levels seen in non-obese (Normal) subjects with no sleep deficits. Obese subjects exhibited significantly higher levels of leptin with sleep deficits compared with non-obese subjects with normal sleep pattern, while obese subjects with SA had significantly high levels of leptin than obese subjects with IN and IN+SA. Patients with sleep deficits had significantly lower levels of serum TRP and zinc than non-obese subjects with normal sleep pattern. Obese subjects with SA had significantly lower levels of zinc and elevated levels of TRP than obese subjects with IN. Obese patients with IN+SA had significantly lower levels of leptin and zinc than IN and SA , while TRP levels were significantly lower in subjects with IN than obese subjects with IN+SA and IN. These results suggest that elevated levels of leptin which are possibly by adiposity and lessened levels of zinc and TRP have a great impact on progression of obesity and their association can contribute to tempt sleep disorders.

Topics: Adiposity; Adult; Biomarkers; Body Mass Index; Case-Control Studies; Cross-Sectional Studies; Female; Humans; Leptin; Male; Obesity; Prognosis; Sleep; Sleep Apnea Syndromes; Sleep Initiation and Maintenance Disorders; Tryptophan; Young Adult; Zinc

Obstructive sleep apnea (OSA) has been associated with increased risk of cardiovascular morbidity and mortality. Although inflammatory markers may mediate this association, it is unknown the influence of gender in this mechanism. Thus, we aimed to evaluate the interaction effects between OSA and gender on metabolic and inflammatory profile in a population sample. This study is part of EPISONO cohort, in which 1042 participants underwent polysomnography, answered questionnaires, and had their blood collected for analysis of fasting glucose, total cholesterol and fractions, leptin, ghrelin, liver transaminases, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and C-reactive protein. The results showed that men with OSA had higher leptin levels, shorter sleep latency and lower N3 sleep stage compared to men control (CTRL). They also presented higher apnea index and number of central apneas compared to both CTRL men and OSA women. In women, OSA was related to longer REM sleep latency, higher apnea-hypopnea index (AHI) during REM sleep and increased TNF-α levels compared to CTRL women. A multivariate model showed that male gender, ghrelin and total cholesterol were negatively associated with TNF-α, while IL-6, triglycerides and hypopnea index were positively associated (R

Topics: Adult; Body Mass Index; Cohort Studies; Cross-Sectional Studies; Female; Ghrelin; Humans; Inflammation; Leptin; Male; Metabolic Diseases; Polysomnography; Sex Characteristics; Sleep Apnea Syndromes; Sleep Stages; Sleep, REM; Socioeconomic Factors; Tumor Necrosis Factor-alpha

Obese leptin-deficient (ob/ob) mice demonstrate defects in upper airway structural and neuromuscular control. We hypothesized that these defects predispose to upper airway obstruction during sleep, and improve with leptin administration. High-fidelity polysomnographic recordings were conducted to characterize sleep and breathing patterns in conscious, unrestrained ob/ob mice (23 wk, 67.2 ± 4.1 g, n = 13). In a parallel-arm crossover study, we compared responses to subcutaneous leptin (1 μg/h) vs. vehicle on respiratory parameters during NREM and REM sleep. Upper airway obstruction was defined by the presence of inspiratory airflow limitation (IFL), as characterized by an early inspiratory plateau in airflow at a maximum level (V̇Imax) with increasing effort. The severity of upper airway obstruction (V̇Imax) was assessed along with minute ventilation (V̇E), tidal volume (VT), respiratory rate (RR), inspiratory duty cycle, and mean inspiratory flow at each time point. IFL occurred more frequently in REM sleep (37.6 ± 0.2% vs. 1.1 ± 0.0% in NREM sleep, P < 0.001), and leptin did not alter its frequency. V̇Imax (3.7 ± 1.1 vs. 2.7 ± 0.8 ml/s, P < 0.001) and V̇E increased (55.4 ± 22.0 vs. 39.8 ± 16.4 ml/min, P < 0.001) with leptin vs. vehicle administration. The increase in V̇E was due to a significant increase in VT (0.20 ± 0.06 vs. 0.16 ± 0.05 ml, P < 0.01) rather than RR. Increases in V̇E were attributable to increases in mean inspiratory flow (2.5 ± 0.8 vs. 1.8 ± 0.6 ml/s, P < 0.001) rather than inspiratory duty cycle. Similar increases in V̇E and its components were observed in non-flow-limited breaths during NREM and REM sleep. These responses suggest that leptin stabilized pharyngeal patency and increased drive to both the upper airway and diaphragm during sleep.

Topics: Animals; Cross-Over Studies; Diaphragm; Leptin; Male; Mice; Mice, Inbred C57BL; Obesity; Pharynx; Polysomnography; Respiratory Function Tests; Respiratory Mechanics; Sleep; Sleep Apnea Syndromes; Sleep, REM

The mechanisms linking sleep disordered breathing with impairment of sleep and bone metabolism/architecture are poorly understood. Here, we explored the role of the neuropeptide orexin, a respiratory homeostasis modulator, in growth retardation induced in an upper airway obstructed (AO) rat model.. The tracheae of 22-day-old rats were narrowed; AO and sham-control animals were monitored for 5 to 7 w. Growth parameters, food intake, sleep/wake activity, and serum hormones were measured. After euthanasia, growth plate (GP) histology, morphometry, orexin receptors (OXR), and related mediators were analyzed. The effect of dual orexin receptor antagonist (almorexant 300 mg/kg) on sleep and GP histology were also investigated.. The AO group slept 32% less; the time spent in slow wave and paradoxical sleep during light period and slow wave activity was reduced. The AO group gained 46% less body weight compared to the control group, despite elevated food intake; plasma ghrelin increased by 275% and leptin level decreased by 44%. The impediment of bone elongation and bone mass was followed by a 200% increase in OX1R and 38% reduction of local GP ghrelin proteins and growth hormone secretagogue receptor 1a. Sry-related transcription factor nine (Sox9), a molecule mediating cartilage ossification, was downregulated and the level of transcription factor peroxisome proliferator-activated receptor gamma was upregulated, explaining the bone architecture abnormalities. Administration of almorexant restored sleep and improved GP width in AO animals.. In AO animals, enhanced expression of orexin and OX1R plays a role in respiratory induced sleep and growth abnormalities.

Topics: Acetamides; Animals; Body Weight; Bone Development; Eating; Ghrelin; Growth Disorders; Homeostasis; Isoquinolines; Leptin; Male; Orexin Receptor Antagonists; Orexin Receptors; Orexins; Rats; Rats, Sprague-Dawley; Respiration; Sleep; Sleep Apnea Syndromes; Sleep, REM; Wakefulness

The study aimed to compare the effect of obesity with and without metabolic syndrome on asthma severity, quality of life, sleep quality, sleep disordered breathing and inflammatory markers as compared to non-obese asthma patients.. 60 asthma patients recruited for the study were divided equally into non-obese (NOA), obese without metabolic syndrome (OANMS) and obese with metabolic syndrome (OAMS) groups. Study cohorts were assessed for severity of asthma, quality of life and quality of sleep using questionnaires and inflammatory markers (FENO, hs-CRP, IL-5, IL-6 and leptin). Institutional ethical committee approved the study.. The results suggests OAMS patients may be a subtype of asthmatics having significantly severe asthma (p < 0.05), poor quality of life (p < 0.05), high risk of OSA (p< 0.05), decreased lung volumes (FRC) (p< 0.05), higher levels of inflammatory markers (leptin and IL-6) (p < 0.05), and high incidence of sleep disordered breathing (p < 0.05) in comparison to NOA and OANMS patients.. The present study has shown that obese asthmatics especially with metabolic syndrome represent a subtype of asthmatic population. Hence, the treatment of metabolic syndrome may be necessary in addition to asthma to achieve optimal control.

Topics: Adolescent; Adult; Asthma; Biomarkers; C-Reactive Protein; Cohort Studies; Cytokines; Female; Humans; Immunoglobulin E; India; Leptin; Male; Metabolic Syndrome; Middle Aged; Nitric Oxide; Obesity; Quality of Life; Severity of Illness Index; Sleep Apnea Syndromes; Surveys and Questionnaires; Young Adult

Over the last 15years, many studies have established an association of sleep apnea with inflammation and metabolic aberrations. However, no controlled studies have examined potential gender effects in this association. We recruited 120 middle-aged, predominantly non-obese mild-to-moderate sleep apneics and controls (62 males, 58 females). All participants underwent a clinical history, physical examination, and 1-night 8-h polysomnography recording and provided a single fasting blood sample for assessment of interleukin-6 (IL-6), tumor necrosis factor receptor 1 (TNFR1), C-reactive protein (CRP), leptin, and adiponectin levels. Among non-sleep apneics, females had higher levels of TNFR1 (p=0.01), CRP (p=0.005), leptin (p<0.001), and adiponectin (p<0.001) compared to males, independent of age and body mass index. When analyzed separately by gender, sleep apneic men had elevated TNFR1 (p=0.04), CRP (p=0.06) and IL-6 (p=0.11) relative to control men; in sleep apneic females, only CRP was elevated (p=0.04). Furthermore, CRP was associated with apnea severity in a dose-response manner (p-linear=0.04 in both genders) and was independently associated with comorbid hypertension in apnea (p-linear=0.005 for women; p-linear=0.09 for men). In conclusion, although women have naturally higher levels of inflammatory and metabolic markers than men, sleep apneic men appear to have a more severe inflammatory profile compared to women. Our findings suggest that these markers should be analyzed and interpreted separately in men and women, and that a single measure of plasma CRP appears to be a clinically-useful marker of apnea severity and comorbid cardiovascular morbidity.

Topics: Adiponectin; C-Reactive Protein; Female; Humans; Inflammation; Interleukin-6; Leptin; Male; Middle Aged; Polysomnography; Receptors, Tumor Necrosis Factor, Type I; Sex Characteristics; Sleep Apnea Syndromes

To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level.. Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3±10.6 (mean±s.d.), body mass index (BMI) 32.7±5.3 kg m(-2) and apnea-hypopnea index 40.2±16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured.. Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30-35 and BMI > or =35 kg m(-2)). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (P=0.04). In post-hoc analysis for nonhypertensive OSA subjects (n=249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (n=199).. Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects.

Topics: Adult; Biomarkers; Body Composition; Body Mass Index; Cohort Studies; Cross-Sectional Studies; Female; Humans; Hypertension; Iceland; Intra-Abdominal Fat; Leptin; Male; Middle Aged; Obesity; Polysomnography; Severity of Illness Index; Sex Distribution; Sleep Apnea Syndromes; Subcutaneous Fat; Surveys and Questionnaires; Time Factors

Sleep deficits associated with sleep apnea and insomnia increase the risk of vascular inflammation and insulin resistance. This study examined the hypothesis that inflammation markers are higher in those diabetic patients who experience sleep deficits compared with those without any history of a sleep disorder.. Fasting blood was obtained after written informed consent, and sleep disorder histories were obtained from type 2 diabetic patients (n=81) attending clinics of the Louisiana State University Health Sciences Center.. There was a significant correlation between body weight and leptin, and leptin in turn was significantly correlated with 10-kDa interferon-γ-induced protein (IP-10) levels and insulin resistance in type 2 diabetic patients. Fasting blood levels of leptin, IP-10, and insulin resistance were significantly elevated in patients with sleep deficits compared with diabetics with normal sleep patterns. There were no differences in glycosylated hemoglobin (HbA1c) or fasting glucose in patients with sleep deficits compared with those with normal sleep patterns. Sleep deficits increase circulating levels of leptin, IP-10, and insulin resistance compared to levels seen in patients with diabetes who reported no difficulty with sleep. Patients with sleep apnea had significantly lower hydrogen sulfide (H(2)S) levels compared with patients with normal sleep patterns or patients with insomnia. Low levels of circulating H(2)S could contribute to higher vascular inflammation in patients with sleep apnea.. These results suggest that sleep apnea is associated with a decrease in circulating H(2)S and sleep disorders increase the risk of inflammation and insulin resistance, which can contribute to the increased risk of vascular disease in subjects with type 2 diabetes.

Topics: Adult; Body Weight; Case-Control Studies; Chemokine CXCL10; Diabetes Mellitus, Type 2; Female; Humans; Hydrogen Sulfide; Insulin Resistance; Leptin; Male; Middle Aged; Sleep Apnea Syndromes; Sleep Initiation and Maintenance Disorders

Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterise the profile of this blood pressure increase, to determine if it is sustained and to explore potential physiological mechanisms. We performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of IH exposure. We also assessed systemic haemodynamics, muscle sympathetic nerve activity (MSNA), ischaemic calf blood flow responses and baroreflex gain. We obtained blood samples for inflammatory markers before, during and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean ± sd MSNA increased across the exposure (17.2 ± 5.1 versus 21.7 ± 7.3 bursts·min⁻¹; p < 0.01) and baroreflex control of sympathetic outflow declined from -965.3 ± 375.1 to -598.4 ± 162.6 AIU·min⁻¹ ·mmHg⁻¹ (p < 0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers. These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from reduced baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.

Topics: Adiponectin; Adult; Blood Pressure; Body Mass Index; C-Reactive Protein; Chemokine CCL5; Female; Humans; Hypertension; Hypoxia; Intercellular Adhesion Molecule-1; Interleukin-8; Leptin; Male; Receptors, Interleukin-1; Sleep Apnea Syndromes; Sympathetic Nervous System; Tumor Necrosis Factor-alpha

Previous research in lean subjects has found lower leptin levels associated with shorter sleep duration. Since leptin levels are higher and some of the actions of leptin are impaired in obese individuals, one cannot assume that sleep will be similarly associated with leptin in obese individuals. The aim of this paper was to examine the cross-sectional association between habitual sleep duration and quality and plasma leptin levels in a sample of 80 obese men and premenopausal women aged 18-50 years. Leptin levels (ng/ml) were assayed on a fasting blood sample taken in the morning. We calculated a relative leptin level by dividing leptin by body fat percentage. Sleep duration and sleep efficiency were measured by 2 weeks of wrist actigraphy and respiratory disturbance index (RDI), a measure of sleep disordered breathing, was assessed by a portable screening device on a single night. Mean leptin levels and body fat percentage were higher in women than men (P < 0.001), however, mean RDI was higher in men (P = 0.01). There were no significant associations between relative leptin level and any of the sleep measures, including sleep duration, sleep efficiency, and sleep disordered breathing. There was also no difference between men and women in the association between sleep and leptin. In conclusion, contrary to what has been reported in other studies, measures of sleep duration and quality were not associated with leptin levels in our sample of obese adults.

Topics: Actigraphy; Adipose Tissue; Adolescent; Adult; Body Composition; Body Mass Index; Cross-Sectional Studies; Fasting; Female; Humans; Leptin; Male; Middle Aged; Obesity; Polysomnography; Premenopause; Sex Factors; Sleep; Sleep Apnea Syndromes; Young Adult

Obstructive sleep apnea disease (OSA) is associated with a myriad of endocrine adverse effects. Changes in the serum prolactin (PRL) secretion in OSA are thought to be related to the hypoxic stress and subsequently to result in reversible changes with effective continuous positive airway pressure (CPAP) therapy. Due to current disagreements on this topic, we investigated the effect of CPAP therapy on the serum PRL in patients with OSA, using the most accurate CPAP compliance assessment to date. Fourteen adults were recruited from those scheduled at the Salem Veterans Affairs Medical Center for a diagnostic polysomnogram (PSG). Fasting serum PRL, estradiol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (Test), glucose, cortisol (Cor), and leptin levels were measured at 7 a.m., the morning after PSG, and again in ten of these patients, after 11-39 months of CPAP therapy. Compliance data, for both short-term (mean, 34 days) and long-term follow-up (mean, 304 days), were downloaded.. Except PRL, no other hormone's serum level, including that of FSH, LH, Test, Cor, and Leptin, has changed significantly after the CPAP therapy.. CPAP therapy is associated with a significant decrease in serum PRL levels.

Topics: Adult; Aged; Blood Glucose; Continuous Positive Airway Pressure; Estradiol; Follicle Stimulating Hormone; Follow-Up Studies; Humans; Hydrocortisone; Infertility, Male; Leptin; Luteinizing Hormone; Male; Middle Aged; Patient Compliance; Prolactin; Sleep Apnea Syndromes; Testosterone

Topics: Abdominal Fat; Acanthosis Nigricans; Adolescent; Atherosclerosis; Bone Diseases, Endocrine; Child; Fatty Liver; Ghrelin; Humans; Hyperandrogenism; Hypertension; Insulin; Insulin Resistance; Leptin; Obesity; Peptide Hormones; Phenotype; Satiation; Sleep Apnea Syndromes

Increasing evidence suggests that alterations in sleep duration are associated with cardiovascular disease (CVD) and mortality. Additionally, sleep disordered breathing (SDB), which is associated with disturbed nighttime sleep and hypoxemia, may be an independent risk factor for CVD. The inflammatory marker, C-reactive protein (CRP), is an important predictor of CVD. We investigated potential associations between circulating CRP, sleep duration, and SDB.. Cross-sectional Study.. Participants were 907 adults from the Wisconsin Sleep Cohort Study (WSCS).. CRP was measured after overnight polysomnography. The relationships between CRP and sleep parameters were evaluated using multiple linear regression with and without controlling for age, sex, and body mass index (BMI) and other potential confounders. CRP was found to be higher for women and had a strong positive correlation with age and BMI. CRP showed a significant positive association with current smoking, waist-hip ratio (WHR), LDL-cholesterol, triglycerides, leptin, and insulin, independent of age, sex, and BMI. Significant independent negative associations for CRP were observed with HDL-cholesterol (HDL), insulin sensitivity (quantitative insulin sensitivity check index [QUICKI]), and hours of exercise. There was a significant positive association between CRP levels and the apnea-hypopnea index (AHI, the measure of SDB), but these relationships were not significant after adjustment for age, sex, and BMI. No significant association between CRP levels and measures of sleep duration (polysomnographic and self-reported) were found.. There was no significant association between CRP levels and sleep duration. The lack of an independent association between CRP levels and SDB suggests that the reported relationship between these 2 variables may be primarily driven by their association with obesity.

Topics: Adult; Blood Glucose; Body Mass Index; C-Reactive Protein; Cardiovascular Diseases; Cohort Studies; Female; Humans; Insulin; Leptin; Life Style; Male; Polysomnography; Risk Factors; Sleep Apnea Syndromes; Smoking; Statistics as Topic; Waist-Hip Ratio

To identify regions on the genome linked to plasma leptin levels.. Full genome scan with 402 microsatellite markers, spaced approximately 10 cM apart. Data were analyzed using the Haseman-Elston regression linkage analysis.. A total of 160 sibling pairs from 59 predominantly African American, obese families recruited to participate in a genetic-epidemiological study of obstructive sleep apnea.. Serum leptin levels adjusted for age, sex, race and body mass index (BMI).. Suggestive linkage peaks were observed on chromosomes 2 (P=0.00170; marker D2S1384), 3 (P=0.00007; marker D3S3034), 4 (P=0.00020; marker D4S1652) and 21 (P=0.00053; marker D21s1411).. The peak on chromosome 3 is near the gene for glycogensynthase kinase 2 beta, an important factor in glucose homeostasis. Linkage was generally stronger after BMI adjustment, suggesting the potential influence of a number of metabolic pathways on leptin levels other than those that directly determine obesity levels. The evidence of linkage for leptin levels is consistent with prior linkage analyses for cholesterol, hypertension and other metabolic phenotypes.

Topics: Adult; Black or African American; Body Mass Index; Chromosome Mapping; Female; Genetic Linkage; Genetic Predisposition to Disease; Humans; Leptin; Male; Microsatellite Repeats; Middle Aged; Ohio; Sleep Apnea Syndromes

Topics: Animals; Humans; Leptin; Obesity; Sleep Apnea Syndromes

Topics: Humans; Hypoventilation; Leptin; Obesity; Sleep Apnea Syndromes; Syndrome

Leptin is a protein hormone produced by fat cells of mammals. It acts within the hypothalamus via a specific receptor to reduce appetite and increase energy expenditure. Plasma leptin levels correlate closely with total body fat mass operating via a central feedback mechanism. In human obesity serum leptin levels are up to four times higher than in lean subjects, indicating a failure of the feedback loop and central leptin resistance. In leptin deficient obese mice (ob/ob mice) leptin infusion reverses hypoventilation. It was hypothesised that a relative deficiency in CNS leptin, indicated by high circulating leptin levels, may be implicated in the pathogenesis of obesity hypoventilation syndrome (OHS).. Fasting morning leptin levels were measured in obese and non-obese patients with and without daytime hypercapnia (n=56). Sleep studies, anthropometric data, spirometric parameters, and awake arterial blood gas tensions were measured in each patient.. In the whole group serum leptin levels correlated closely with % body fat (r=0.77). Obese hypercapnic patients (mean (SD) % body fat 43.8 (6.0)%) had higher fasting serum leptin levels than eucapnic patients (mean % body fat 40.8 (6.2)%), with mean (SD) leptin levels of 39.1 (17.9) and 21.4 (11.4) ng/ml, respectively (p<0.005). Serum leptin (odds ratio (OR) 1.12, 95% CI 1.03 to 1.22) was a better predictor than % body fat (OR 0.92, 95% CI 0.76 to 1.1) for the presence of hypercapnia.. Hyperleptinaemia is associated with hypercapnic respiratory failure in obesity. Treatment with leptin or its analogues may have a role in OHS provided central leptin resistance can be overcome.

Topics: Adult; Aged; Aged, 80 and over; Carbon Dioxide; Female; Humans; Hypoventilation; Leptin; Male; Middle Aged; Obesity; Partial Pressure; Regression Analysis; Sleep Apnea Syndromes

To investigate the possible associations between sleep apnea syndrome, hyperinsulinemia/insulin resistance and hyperleptinemia in subjects with different degrees of body mass index.. To test for the presence or absence of sleep apnea syndrome in association with hyperinsulinemia/insulin resistance and hyperleptinemia.. Twenty subjects with different body mass index (mean BMI 30.9+/-4.2).. Insulin action and plasma soluble leptin receptor were measured by euglycemic hyperinsulinemic glucose clamp and by ELISA method, respectively. Occurrence of sleep apnea syndrome was assessed by clinical and nocturnal monitoring using a validated sleep apnea recorder.. The apnea/hypopnea index (AHI) was positively correlated with plasma soluble leptin receptor (0.76; P<0.001) and negatively with the degree of insulin-mediated glucose uptake (r=-0.73; P<0.001). In a multivariate analysis AHI was associated with plasma soluble leptin receptor and insulin mediated glucose uptake independently of age, gender, BMI, plasma leptin levels and PaCO(2).. Sleep apnea syndrome is associated with plasma soluble leptin receptor and insulin resistance independently of BMI.

Topics: Adult; Body Mass Index; Carbon Dioxide; Carrier Proteins; Enzyme-Linked Immunosorbent Assay; Female; Glucose Clamp Technique; Humans; Insulin; Insulin Resistance; Leptin; Male; Middle Aged; Receptors, Cell Surface; Receptors, Leptin; Sleep Apnea Syndromes; Solubility; Triglycerides

The control of body weight and cardiac sympathetic function in patients with obstructive sleep apnoea-hypopnoea syndrome (OSAHS) are important because both factors have significant effects on the mortality of these patients. It has recently been reported that OSAHS has a significant effect on the secretion of leptin, a hormone involved in the control of body weight and sympathetic nerve activity. In addition to the circadian rhythm of leptin secretion, the effects of one night of treatment with nasal continuous positive airway pressure (nCPAP) and the mechanism of the effects of nCPAP on nocturnal leptin secretion in patients with OSAHS has not yet been elucidated.. Blood samples were obtained at 21.00 hours, 00.00 hours, 03.00 hours, and 06.30 hours from 21 subjects with OSAHS (mean apnoea and hypopnoea index 52.4/h), with and without nCPAP treatment. Iodine-123 (I(123))-meta-iodobenzylguanidine (MIBG) imaging was used to evaluate myocardial sympathetic function before nCPAP treatment.. Plasma leptin reached a peak level at 00:00 hours (p<0.01) in patients with OSAHS, both with and without nCPAP treatment. The first night of nCPAP treatment significantly decreased the plasma leptin levels at 03.00 hours (without nCPAP: mean (SE) 21.6 (4.7) ng/ml; with nCPAP: 19.3 (4.1) ng/ml, p<0.02) and at 06.30 hours (without nCPAP: 17.6 (3.8) ng/ml; with nCPAP: 15.2 (3.2) ng/ml, p<0.01). The magnitude of the decrease in leptin levels after nCPAP treatment was significantly correlated with cardiac sympathetic function measured before nCPAP treatment (p<0.03).. Patients with OSAHS undergo nocturnal increases in leptin levels in spite of interruption of sleep due to apnoea and hypopnoea, a trend seen in normal subjects. Plasma leptin levels in patients with OSAHS decreased significantly after the first night of nCPAP treatment. Enhanced cardiac sympathetic function in these patients may contribute to the leptin levels before nCPAP treatment and vice versa.

Topics: 3-Iodobenzylguanidine; Adult; Aged; Autonomic Nervous System Diseases; Blood Glucose; Heart Diseases; Humans; Insulin; Leptin; Male; Middle Aged; Positive-Pressure Respiration; Radionuclide Imaging; Sleep Apnea Syndromes

Obstructive sleep apnea syndrome (OSAS) is a common disorder in obese subjects. Visceral fat accumulation (VFA) is a better predictor of coronary heart disease than body mass index. Leptin is a hormone involved in the control of body weight and fat distribution. The effect of nasal continuous positive airway pressure (NCPAP) treatment on VFA and serum leptin levels in OSAS patients has not been known.. VFA and subcutaneous fat accumulation (SFA) were assessed by CT before and after NCPAP treatment in 22 OSAS patients (mean apnea and hypopnea index >50 episodes/h). Serum leptin levels of another 21 OSAS patients were measured before and after 3 to 4 days of NCPAP to gain insight into the mechanism by which NCPAP affects fat distribution. VFA and SFA decreased significantly after 6 months of NCPAP treatment (236+/-16 to 182+/-14cm(2), P=0.0003 and 215+/-21 to 189+/-18 cm(2), P=0.003, respectively). VFA decreased significantly in the body weight reduction group (n=9, P<0.01) and the no body weight reduction group (n=13, P<0.03). In contrast, SFA changed significantly in the body weight reduction group only (P<0.01). Leptin levels decreased significantly following 3 to 4 days of NCPAP (P<0.01), whereas body weight, fasting insulin, and cortisol levels did not change significantly.. Correction of sleep disordered breathing by NCPAP may be used to reduce VFA in OSAS patients. OSAS may have significant effects on the serum leptin levels.

Topics: Adipose Tissue; Blood Glucose; Body Weight; Cholesterol, LDL; Glucose Tolerance Test; Leptin; Positive-Pressure Respiration; Proteins; Sleep Apnea Syndromes; Triglycerides; Viscera; Weight Loss