Study of the relationship between the interleukin-6 gene and obstructive sleep apnea.
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ABSTRACT:
SUBMITTER: Larkin EK
PROVIDER: S-EPMC3078635 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Obstructive sleep apnea (OSA) is a common sleep disorder, effecting 17% of the total population and 40-70% of the obese population (1, 2). Multiple studies have identified OSA as a critical risk factor for the development of obesity, diabetes, and cardiovascular diseases (3-5). Moreover, emerging evidence indicates that metabolic disorders can exacerbate OSA, creating a bidirectional relationship between OSA and metabolic physiology. In this review, we explore the relationship between glycemic control, insulin, and leptin as both contributing factors and products of OSA. We conclude that while insulin and leptin action may contribute to the development of OSA, further research is required to determine the mechanistic actions and relative contributions independent of body weight. In addition to increasing our understanding of the etiology, further research into the physiological mechanisms underlying OSA can lead to the development of improved treatment options for individuals with OSA.
| S-EPMC6087747 | biostudies-literature
Project description:Study objectivesThe role of obstructive sleep apnea (OSA) in the overall outcome of ruptured intracranial aneurysms (RIAs) is unknown. We have investigated the role of OSA in overall outcome of RIAs.MethodsData from 159 consecutive patients were retrospectively reviewed. A chi-square test and regression analysis were performed to determine the significant difference. A value of P < .05 was considered significant.ResultsThe prevalence of OSA in RIAs was fivefold higher in the nonaneurysm patient group, P = .002. The number of patients with hypertension (P < .0001), body mass index ≥ 30 (P < .0001), hyperlipidemia (P = .018), chronic heart disease (P = .002) or prior ischemic stroke (P = .001) was significantly higher in the OSA group. Similarly, the number of wide-neck aneurysms (P < .0001) and aneurysm > 7 mm (P = .004), poor Hunt and Hess grade IV-V (P = .005), vasospasms, (P = .03), and patients with poor Modified Rankin Scale scores (3-6) was significantly higher in the OSA group (P < .0001). Interestingly, for the first time in univariate (P = .01) and multivariate (P = .003) regression analysis, OSA was identified as an individual predictor of unfavorable outcome of RIAs. In addition, hypertension (P = .04), smoking (P = .049), chronic heart disease (P = .01), and Hunt and Hess grade IV-V (P = .04) were revealed as predictors of poor outcome of RIAs.ConclusionsThis is a novel study to determine the association between OSA and ruptured cerebral aneurysm in terms of comorbidities, size of aneurysm, severity of symptoms, and outcomes after treatment. In addition, for the first time, OSA is identified as a positive predictor of unfavorable outcome of RIAs.
| S-EPMC7099178 | biostudies-literature
Project description:In obstructive sleep apnea (OSA), recurrent upper airway obstruction and apnea/hypopnea episodes result in endothelial dysfunction, which leads to the release of many proinflammatory cytokines and reactive oxygen species (ROS). ROS induces NLRP3, a protein involved in the synthesis of interleukin (IL)-1 and IL-18; vaspin is a serine protease inhibitor that has an important role in suppressing the activation of NLRP3 inflammasome. In this study, we aimed to investigate the effect of NLRP3 rs10159239 (rs9239) and vaspin rs2236242 (rs6242) single nucleotide polymorphisms (SNPs) on OSA development. This study included 220 individuals who underwent polysomnography (118 patients with OSA and 102 healthy controls). NLRP3 rs9239 and vaspin rs6242 mutation frequencies were analyzed. The NLRP3 rs9239 SNP genotype analysis revealed no statistically significant differences between the OSA and control groups. In the vaspin gene analysis, the rs6242 AA genotype was significantly more frequent in the OSA group compared with the control group, while the AT genotype was more frequent in controls (P = 0.004, P = 0.02). Comparison of rs6242 allele levels showed that the A allele was significantly more frequent in OSA patients than in controls (P = 0.03). The AA genotype was significantly more frequent in patients with severe OSA than in patients with mild or moderate OSA and the control group (P = 0.001 for all). Serum vaspin levels were significantly lower in carriers of the AA genotype than those with AT and TT genotypes (P = 0.001). The vaspin rs6242 SNP AA genotype increased susceptibility to OSA, while the AT genotype appeared to be protective. The lower plasma vaspin levels in OSA compared with the control group and in patients with the AA genotype suggest that vaspin may be a protective biomarker for OSA.
| S-EPMC8276347 | biostudies-literature
Project description:Obstructive sleep apnea (OSA) is the most common sleep disorder. Sleep bruxism (SB) is a masticatory muscle activity during sleep that commonly co-occurs with OSA. The presented study aimed to assess this relationship and to identify factors affecting this co-occurrence. Adult patients (n = 110) were evaluated for OSA and SB in a sleep laboratory using polysomnography. The episodes of bruxism and respiratory events were scored according to the standards of the American Academy of Sleep Medicine. The prevalence of OSA and SB was found to be 86.37% and 50%, respectively. The bruxism episode index (BEI) was increased in the group with mild and moderate OSA (apnea-hypopnea index (AHI) <30) compared to that in the group with severe OSA (AHI ? 30) (5.50 ± 4.58 vs. 1.62 ± 1.28, p < 0.05). A positive correlation between AHI and BEI was observed in the group with AHI < 30. Regression analysis indicated that higher AHI, male gender, and diabetes were independent predictors for the increased BEI in group with AHI < 30. The relationship between OSA and SB depends on the degree of severity of OSA. OSA is correlated with SB in mild and moderate cases of OSA in the group of patients with increased risk of OSA.
| S-EPMC6832407 | biostudies-literature
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-M-NM-:B pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder. Total RNA from visceral fat of 18 subjects (10 OSA, 8 Control) was hybridized to 18 Affymetrix Genechip Human Gene 1.0 ST microarrays.
2012-09-01 | E-GEOD-38792 | biostudies-arrayexpress
Project description:In recent years, growing evidence suggests an association between obstructive sleep apnea (OSA), a common sleep breathing disorder which is increasing in prevalence as the obesity epidemic surges, and atrial fibrillation (AF), the most common cardiac arrhythmia. AF is a costly public health problem increasing a patient's risk of stroke, heart failure, and all-cause mortality. It remains unclear whether the association is based on mutual risk factors, such as obesity and hypertension, or whether OSA is an independent risk factor and causative in nature. This paper explores the pathophysiology of OSA which may predispose to AF, clinical implications of stroke risk in this cohort who display overlapping disease processes, and targeted treatment strategies such as continuous positive airway pressure and AF ablation.
| S-EPMC3600315 | biostudies-other
Project description:Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia and associated with the disruption of circadian rhythm. The study aimed to assess the relationship between hypoxia-inducible factor (HIF) subunits, circadian clock proteins, and polysomnography (PSG) variables, in healthy individuals and severe OSA patients. The study included 20 individuals, who underwent PSG and were divided into severe OSA group (n = 10; AHI ? 30) and healthy control (n = 10; AHI < 5) based on apnea-hypopnea index (AHI). All participants had their peripheral blood collected in the evening before and the morning after the PSG. HIF-1?, HIF-1?, BMAL1, CLOCK, CRY1, and PER1 protein concertation measurements were performed using ELISA. In a multivariate general linear model with the concentration of all circadian clock proteins as dependent variables, evening HIF-1? protein level was the only significant covariant (p = 0.025). Corrected models were significant for morning and evening PER1 (p = 0.008 and p = 0.006, respectively), evening (p = 0.043), and evening BMAL protein level (p = 0.046). In corrected models, evening HIF-1? protein level had an influence only on the evening PER1 protein level. Results suggest that OSA patients are at risk for developing circadian clock disruption. This process might be mediated by subunit ? of HIF-1, as its increased protein level is associated with overexpression of circadian clock proteins.
| S-EPMC7291176 | biostudies-literature
Project description:IntroductionAlthough psoriasis and obstructive sleep apnea syndrome (OSAS) are associated with systemic inflammation, studies on their potential bilateral relationship are not sufficient.AimTo investigate vitamin D levels and receptor gene polymorphisms in patients with OSAS and psoriasis and the associations with these diseases.Material and methodsOne hundred thirty-seven patients included in the study consisted of 4 different groups: group 1, those with both diseases; group 2, those with OSAS only; group 3, patients with psoriasis only; and group 4, healthy controls. The patients' serum calcium, phosphorus, AHI, Epworth Sleepiness Scale, Psoriasis Area Severity Index, and VDR TagI, ApaI, BsmI polymorphisms were compared.ResultsVitamin D levels of groups 1, 2 and 3 were found to be lower than in controls. There was no statistically significant correlation between VDR TagI, ApaI, BsmI gene polymorphisms of the groups. Vitamin D levels were significantly higher in patients with heterozygous ApaI genotype (A/C) compared to patients with normal (A/A) or homozygous mutant (C/C) genotype (p < 0.05). No relationship was determined between VDR TagI, ApaI, BsmI, and the other parameters.ConclusionsIn our study, 1,25(OH)2-vitamin D3 levels were significantly lower in all disease groups compared to the control group. Although there is no difference between the groups in terms of VDR gene polymorphism, we think that there may be a bidirectional relationship between these diseases based on the low vitamin D levels.
| S-EPMC9131946 | biostudies-literature
Project description:This review offers an overview of the relationship between diabetes, obstructive sleep apnea (OSA), obesity, and heart disease. It then addresses evidence that the traditional understanding of this relationship is incomplete or misleading. In the process, there is a brief discussion of the evolutionary rationale for the development and retention of OSA in light of blood sugar dysregulation, as an adaptive mechanism in response to environmental stressors, followed by a brief overview of the general concepts of epigenetics. Finally, this paper presents the results of a literature search on the epigenetic marks and changes in gene expression found in OSA and diabetes. (While some of these marks will also correlate with obesity and heart disease, that is beyond the scope of this project). We conclude with an exploration of alternative explanations for the etiology of these interlinking diseases.
| S-EPMC8945691 | biostudies-literature
Project description:Rationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses. Methods: Patients scheduled to undergo ventral hernia repair surgery were recruited to wear a portable home sleep monitor for two nights prior to surgery. Visceral fat biopsies were obtained intra-operatively. RNA was extracted and whole-genome expression profiling was performed. Gene Set Enrichment Analysis (GSEA) was used to identify curated gene sets that were differentially enriched in OSA subjects. Network analysis was applied to a select set of highly enriched pathways. Results: 10 patients with OSA and 8 control subjects were recruited. There were no differences in age, gender, body mass index between the two groups, but the OSA subjects had a significantly higher respiratory disturbance index (19.2 vs. 0.6, P-value 0.05) and worse hypoxemia (minimum oxygen saturation 79.7% vs. 87.8%, P-value < 0.001). GSEA identified a number of gene sets up-regulated in adipose tissue of OSA patients including the pro-inflammatory NF-κB pathway and the proteolytic ubiquitin/proteasome module. A critical metabolic pathway, the peroxisome proliferator-activated receptor (PPAR), was down-regulated in subjects with OSA. Network analysis linked members of these modules together and identified regulatory hubs. Conclusions: OSA is associated with alterations in visceral fat gene expression. Pathway-based network analysis highlighted perturbations in several key pathways whose coordinated interactions may contribute to the metabolic dysregulation observed in this complex disorder.
2012-09-01 | GSE38792 | GEO