Interaction between obstructive sleep apnea and short sleep duration on insulin resistance: a large-scale study : OSA, short sleep duration and insulin resistance.
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ABSTRACT:
SUBMITTER: Xu H
PROVIDER: S-EPMC7298870 | biostudies-literature | 2020 Jun
REPOSITORIES: biostudies-literature
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Interaction between obstructive sleep apnea and short sleep duration on insulin resistance: a large-scale study : OSA, short sleep duration and insulin resistance.
Xu Huajun H Liang Chen C Zou Jianyin J Yi Hongliang H Guan Jian J Gu Meizhen M Feng Yanhong Y Yin Shankai S
Respiratory research 20200616 1
<h4>Objectives</h4>Both short sleep duration and obstructive sleep apnea (OSA) seem to be associated with insulin resistance. We aimed to explore whether short sleep duration modifies the relationship between OSA and insulin resistance.<h4>Methods</h4>Participants were consecutively enrolled from our sleep center during the period from 2007 to 2017. The index of homeostasis model assessment insulin resistance (HOMA-IR) was calculated from insulin and glucose. Sleep duration was determined by sta ...[more]
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Project description:RationaleObstructive sleep apnea is associated with insulin resistance and liver injury. It is unknown whether apnea contributes to insulin resistance and steatohepatitis in severe obesity.ObjectivesTo examine whether sleep apnea and nocturnal hypoxemia predict the severity of insulin resistance, systemic inflammation, and steatohepatitis in severely obese individuals presenting for bariatric surgery.MethodsWe performed sleep studies and measured fasting blood glucose, serum insulin, C-reactive protein, and liver enzymes in 90 consecutive severely obese individuals, 75 women and 15 men, without concomitant diabetes mellitus or preexistent diagnosis of sleep apnea or liver disease. Liver biopsies (n = 20) were obtained during bariatric surgery.Measurements and main resultsObstructive sleep apnea with a respiratory disturbance index greater than 5 events/hour was diagnosed in 81.1% of patients. The median respiratory disturbance index was 15 +/- 29 events/hour and the median oxygen desaturation during apneic events was 4.6 +/- 1.8%. All patients exhibited high serum levels of C-reactive protein, regardless of the severity of apnea, whereas liver enzymes were normal. Oxygen desaturation greater than 4.6% was associated with a 1.5-fold increase in insulin resistance, according to the homeostasis model assessment index. Histopathology data suggested that significant nocturnal desaturation might predispose to hepatic inflammation, hepatocyte ballooning, and liver fibrosis. Fasting blood glucose levels and steatosis scores were not affected by nocturnal hypoxia. There was no relationship between the respiratory disturbance index and insulin resistance or liver histopathology.ConclusionsHypoxic stress of sleep apnea may be implicated in the development of insulin resistance and steatohepatitis in severe obesity.
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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:BackgroundObstructive sleep apnea (OSA) causes high morbidity and mortality and is independently associated with an increased likelihood of multiple complications. The diagnosis of OSA is presently time-consuming, labor-intensive and inaccessible.AimThis study sought to develop a simple and efficient model for identifying OSA in Chinese adult population.MethodsIn this study, the efficiency of Epworth Sleepiness Scale (ESS) and a new established prediction model for screening OSA were evaluated in the test cohort (2,032 participants) and confirmed in an independent validation cohort (784 participants).ResultsIn the test cohort, a high specificity (82.77%, 95% confidence interval [CI], 77.36-87.35) and a moderate sensitivity (61.65%, 95% CI, 59.35-63.91) were obtained at the threshold of nine for the ESS alone. Notably, sex-stratified analysis revealed different optimum cut-off points: nine for males and six for females. The new generated screening model, including age, waist circumference, ESS score, and minimum oxygen saturation (SaO2) as independent variables, revealed a higher sensitivity (89.13%, 95% CI, 87.60-90.53) and specificity (90.34%, 95% CI, 85.85-93.77) at the best cut-off point. Through receiver operating characteristics curve analysis, the area under the receiver operating characteristics curve of the model was found significantly larger than that of the ESS alone (0.955 vs. 0.774, P<0.0001). All these results were confirmed in the validation cohort.ConclusionsA practical screening model comprising minimum SaO2 and other parameters could efficiently identify undiagnosed OSA from the high-risk patients. Additionally, a sex-specific difference should be considered if the ESS alone is used.
| S-EPMC3846620 | 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
Project description:Obstructive sleep apnea (OSA) is a common disorder characterized by the reduction or complete cessation in airflow resulting from an obstruction of the upper airway. Several studies have observed an increased risk for cardiovascular morbidity and mortality among OSA patients. Metabolic syndrome (MetS), a cluster of cardiovascular risk factors characterized by the presence of insulin resistance, is often found in patients with OSA, but the complex interplay between these two syndromes is not well understood. In this study, we present the results of a genetic association analysis of 373 candidate SNPs for MetS selected in a previous genome wide association analysis (GWAS). The 384 selected SNPs were genotyped using the Illumina VeraCode Technology in 387 subjects retrospectively assessed at the Internal Medicine Unit of the "Virgen de Valme" University Hospital (Seville, Spain). In order to increase the power of this study and to validate our findings in an independent population, we used data from the Framingham Sleep Study which comprises 368 individuals. Only the rs11211631 polymorphism was associated with OSA in both populations, with an estimated OR=0.57 (0.42-0.79) in the joint analysis (p=7.21×10(-4)). This SNP was selected in the previous GWAS for MetS components using a digenic approach, but was not significant in the monogenic study. We have also identified two SNPs (rs2687855 and rs4299396) with a protective effect from OSA only in the subpopulation with abdominal obesity. As a whole, our study does not support the idea that OSA and MetS share major genetic determinants, although both syndromes share common epidemiological and clinical features.
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Project description:Prevalence of cardiovascular disease (CVD) is increased in patients with obstructive sleep apnea (OSA), possibly related to dyslipidemia in these individuals. Insulin resistance is also common in OSA, but its contribution to dyslipidemia of OSA is unclear. The study's aim was to define the relationships among abnormalities of lipoprotein metabolism, clinical measures of OSA, and insulin resistance.Cross-sectional study. OSA severity was defined by the apnea-hypopnea index (AHI) during polysomnography. Hypoxia measures were expressed as minimum and mean oxygen saturation, and the oxygen desaturation index. Insulin resistance was quantified by determining steady-state plasma glucose (SSPG) concentrations during the insulin suppression test. Fasting plasma lipid/lipoprotein evaluation was performed by vertical auto profile methodology.Academic medical center.107 nondiabetic, overweight/obese adults.Lipoprotein particles did not correlate with AHI or any hypoxia measures, nor were there differences noted by categories of OSA severity. By contrast, even after adjustment for age, sex, and BMI, SSPG was positively correlated with triglycerides (r = 0.30, P < 0.01), very low density lipoprotein (VLDL) and its subclasses (VLDL1+2) (r = 0.21-0.23, P < 0.05), and low density lipoprotein subclass 4 (LDL4) (r = 0.30, P < 0.01). SSPG was negatively correlated with high density lipoprotein (HDL) (r = -0.38, P < 0.001) and its subclasses (HDL2 and HDL3) (r = -0.32, -0.43, P < 0.01), and apolipoprotein A1 (r = -0.33, P < 0.01). Linear trends of these lipoprotein concentrations across SSPG tertiles were also significant.Pro-atherogenic lipoprotein abnormalities in obstructive sleep apnea (OSA) are related to insulin resistance, but not to OSA severity or degree of hypoxia. Insulin resistance may represent the link between OSA-related dyslipidemia and increased cardiovascular disease risk.
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Project description:BackgroundStudies demonstrate an association between vitamin D (25(OH)D) deficiency and sleep disturbances, such as obstructive sleep apnea (OSA) and short sleep duration. However, to date, no studies have concurrently and objectively evaluated the effect of these factors on 25(OH)D.ObjectivesTo evaluate whether OSA and objective short sleep duration are independently associated with reduced 25(OH)D in an adult population sample.MethodsA cross-sectional study included 657 individuals from the city of Sao Paulo, Brazil, as part of the ERA project. Participants fulfilled questionnaires and underwent clinical evaluation, polysomnography and blood sample collection for 25(OH)D quantification. OSA was classified into three categories (mild, moderate and severe). The risk of 25(OH)D deficiency was considered as levels<30 ng/mL. Short sleep duration was defined as total sleep time<6 hours.ResultsThe risk of 25(OH)D deficiency was observed in 59.5% of the sample, affecting more individuals of the female gender, obese, with African American ethnicity, and those that were smokers, sedentary and presented hypertension and diabetes. In the final logistic model adjusted for age, gender, ethnicity, obesity, smoking, hypertension, diabetes, sedentary lifestyle, seasonality and creatinine serum levels, both OSA and short sleep duration showed significant independent associations with the risk of 25(OH)D deficiency (moderate OSA: OR for 25(OH)D<30 = 2.21, 95% CI: 1.35-3.64, p<0.01; severe OSA: OR for 25(OH)D<30 = 1.78, 95% CI: 1.06-3.00, p = 0.03; short sleep duration: OR for 25(OH)D<30 = 1.61, 95% CI: 1.15-2.26, p = 0.01). After a subgroup analysis, similar results were observed only in participants ?50 years.ConclusionOSA and short sleep duration are independently associated with the risk of 25(OH)D deficiency in an adult population. Age-related changes in vitamin D metabolism and the frequency of sleep disorders may be involved in these associations. Future studies exploring whether 25(OH)D levels may modulate OSA and sleep curtailment-related outcomes are needed.
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Project description:PurposeDiscrepancies between subjective and objective measures of total sleep time (TST) are frequent among insomnia patients, but this issue remains scarcely investigated in obstructive sleep apnea (OSA). We aimed to evaluate if sleep perception is affected by the severity of OSA.MethodsWe performed a 3-month cross-sectional study of Brazilian adults undergoing overnight polysomnography (PSG). TST was objectively assessed from PSG and by a self-reported questionnaire (subjective measurement). Sleep perception index (SPI) was defined by the ratio of subjective and objective values. Diagnosis of OSA was based on an apnea/hypopnea index (AHI) ≥ 5.0/h, being its severity classified according to AHI thresholds: 5.0-14.9/h (mild OSA), 15.0-29.9/h (moderate OSA), and ≥ 30.0/h (severe OSA).ResultsOverall, 727 patients were included (58.0% males). A significant difference was found in SPI between non-OSA and OSA groups (p = 0.014). Mean SPI values significantly decreased as the OSA severity increased: without OSA (100.1 ± 40.9%), mild OSA (95.1 ± 24.6%), moderate OSA (93.5 ± 25.2%), and severe OSA (90.6 ± 28.2%), p = 0.036. Using logistic regression, increasing SPI was associated with a reduction in the likelihood of presenting any OSA (p = 0.018), moderate/severe OSA (p = 0.019), and severe OSA (p = 0.028). However, insomnia was not considered as an independent variable for the presence of any OSA, moderate/severe OSA, and severe OSA (all p-values > 0.05).ConclusionIn a clinical referral cohort, SPI significantly decreases with increasing OSA severity, but is not modified by the presence of insomnia symptoms.
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Project description:BackgroundObstructive sleep apnea (OSA) is a common sleep disorder associated with several adverse health outcomes. Given the close association between OSA and obesity, lifestyle and dietary interventions are commonly recommended to patients, but the evidence for their impact on OSA has not been systematically examined.ObjectivesTo conduct a systematic review and meta-analysis to assess the impact of weight loss through diet and physical activity on measures of OSA: apnea-hypopnea index (AHI) and oxygen desaturation index of 4% (ODI4).MethodsA systematic search was performed to identify publications using Medline (1948-2011 week 40), EMBASE (from 1988-2011 week 40), and CINAHL (from 1982-2011 week 40). The inverse variance method was used to weight studies and the random effects model was used to analyze data.ResultsSeven randomized controlled trials (519 participants) showed that weight reduction programs were associated with a decrease in AHI (-6.04 events/h [95% confidence interval -11.18, -0.90]) with substantial heterogeneity between studies (I(2) = 86%). Nine uncontrolled before-after studies (250 participants) showed a significant decrease in AHI (-12.26 events/h [95% confidence interval -18.51, -6.02]). Four uncontrolled before-after studies (97 participants) with ODI4 as outcome also showed a significant decrease in ODI4 (-18.91 episodes/h [95% confidence interval -23.40, -14.43]).ConclusionsPublished evidence suggests that weight loss through lifestyle and dietary interventions results in improvements in obstructive sleep apnea parameters, but is insufficient to normalize them. The changes in obstructive sleep apnea parameters could, however, be clinically relevant in some patients by reducing obstructive sleep apnea severity. These promising preliminary results need confirmation through larger randomized studies including more intensive weight loss approaches.
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