ArticleNature and science of sleep2024
Obstructive Sleep Apnea Syndrome and Obesity Indicators, Circulating Blood Lipid Levels, and Adipokines Levels: A Bidirectional Two-Sample Mendelian Randomization Study.
Article in Nature and science of sleep, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Causal effects of life-course obesity on sleep apnoea: a Mendelian randomization study.Internal and emergency medicine · 2026Article
- Prevalence of Positive Screening of Sleep-Disordered Breathing Among Children and Adolescents in Orthodontic Settings: A Systematic Review.Journal of clinical medicine · 2026Review
- Serum asprosin levels in obstructive sleep apnea syndrome: relationship with disease severity and adipose tissue distribution.Sleep & breathing = Schlaf & Atmung · 2026Observational
- [The value of tonsil ultrasound measurement in pediatric obstructive sleep apnea].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2026Article
- TEX10: A Novel Drug Target and Potential Therapeutic Direction for Sleep Apnea Syndrome.Nature and science of sleep · 2025Article
- Causal Relationship Between Childhood Obesity and Sleep Apnea Syndrome: Bidirectional Two-Sample Mendelian Randomization Analysis.Nature and science of sleep · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Purpose: This investigation sought to elucidate the genetic underpinnings that connect obesity indicators, circulating blood lipid levels, adipokines levels and obstructive sleep apnea syndrome (OSAS), employing a bidirectional two-sample Mendelian randomization (MR) analysis that utilizes data derived from extensive genome-wide association studies (GWAS). Methods: We harnessed genetic datasets of OSAS available from the FinnGen consortium and summary data of four obesity indices (including neck circumference), seven blood lipid (including triglycerides) and eleven adipokines (including leptin) from the IEU OpenGWAS database. We primarily utilized inverse variance weighted (IVW), weighted median, and MR-Egger methods, alongside MR-PRESSO and Cochran's Q tests, to validate and assess the diversity and heterogeneity of our findings. Results: After applying the Bonferroni correction, we identified significant correlations between OSAS and increased neck circumference (Odds Ratio [OR]: 3.472, 95% Confidence Interval [CI]: 1.954-6.169, P= 2.201E-05) and decreased high-density lipoprotein (HDL) cholesterol levels (OR: 0.904, 95% CI: 0.858-0.952, P= 1.251E-04). Concurrently, OSAS was linked to lower leptin levels (OR: 1.355, 95% CI: 1.069-1.718, P= 0.012) and leptin receptor levels (OR: 0.722, 95% CI: 0.530-0.996, P= 0.047). Sensitivity analyses revealed heterogeneity in HDL cholesterol and leptin indicators, but further multiplicative random effects IVW method analysis confirmed these correlations as significant (P< 0.05) without notable heterogeneity or horizontal pleiotropy in other instrumental variables. Conclusion: This investigation compellingly supports the hypothesis that OSAS could be a genetic predisposition for elevated neck circumference, dyslipidemia, and adipokine imbalance. These findings unveil potential genetic interactions between OSAS and metabolic syndrome, providing new pathways for research in this domain. Future investigations should aim to delineate the specific biological pathways by which OSAS impacts metabolic syndrome. Understanding these mechanisms is critical for developing targeted prevention and therapeutic strategies.
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