Effect of smoking behaviour and related blood DNA methylation on visceral adipose tissues
Authors' conclusion
Our study uncovered a significant causal effect between smoking and VATs, with T2DM identified as a potential mediator. Further investigation into DNA methylation yielded novel insights into the pathogenic role of smoking on EPAT.
Study context
- Comparison
- Genetically proxied smoking behaviours and smoking-related DNA methylation vs visceral adipose tissues
- Outcome
- Visceral adipose tissues: epicardial and pericardial adipose tissue (EPAT), liver fat (LF), pancreas fat (PF)
Methodological detailsunivariable Mendelian randomization (MR), mediation MR, summary-data-based MR (SMR), colocalization analysis
- Univariable MR
- Mediation MR
- Summary-data-based MR (SMR)
- Colocalization analysis
Main finding
As reported in the abstract
- Smoking initiation and increased epicardial and pericardial adipose tissue (EPAT): beta 0.15, 95% CI 0.06, 0.23, p = 7.01 × 10-4
- Smoking initiation and increased liver fat (LF) area: beta 0.15, 95% CI 0.05, 0.24, p = 2.85 × 10-3
Further findings
Mediation
- T2D suggested as a potential mediator
Smoking-related DNA methylation and EPAT
- WT1 methylation at cg05222924 and lower EPAT area: beta −0.12, 95% CI −0.16, −0.06, PFDR = 2.24 × 10-3
- GPX1 methylation at cg18642234 and EPAT deposition: beta 0.15, 95% CI 0.10, 0.20, PFDR = 1.66 × 10-4
Original publication
Effect of smoking behaviour and related blood DNA methylation on visceral adipose tissues. Diabetes Obes Metab. Published 7 November 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →