Lipids & metabolic liver disease
Visceral adipose tissue and risk of nonalcoholic fatty liver disease: A Mendelian randomization study
Authors' conclusion
This study provided genetic evidence that higher VAT mass causally associated with a higher risk of NAFLD. The amount of VAT could be reduced using a therapeutic strategy for managing NAFLD.
Study context
- Population
- SNPs associated with visceral adipose tissue (VAT) from GWAS; Nonalcoholic fatty liver disease (NAFLD) summary-level data from FinnGen consortium (2275 cases and 375,002 controls)2,275 NAFLD cases · 375,002 controls · GWAS 325,153
- Comparison
- Genetically predicted higher VAT mass vs lower VAT mass
- Outcome
- NAFLD risk per genetically predicted VAT mass (IVW method)
Methodological detailsrandom-effects inverse-variance weighted (IVW) main Mendelian randomization (MR) approach, weighted median and MR-Egger alternate methods, sensitivity analyses
- Random-effects inverse-variance weighted (IVW) main MR approach
- Weighted median and MR-Egger alternate methods
- Sensitivity analyses
Main finding
As reported in the abstract
NAFLD risk per genetically predicted higher VAT mass
IVW (main): β = 0.665, OR (95% CI 1.482-2.550), p = 1.58e-06
1.944
Further findings
NAFLD risk, alternate MR methods
- Weighted median (WM): β = 0.615, OR (95% CI 1.272-2.689), p = 1.29e-03
- 1.849
- MR-Egger: β = 1.250, OR (95% CI 1.522-7.998), p = 3.52e-03
- 3.490
Sensitivity analysis
- Heterogeneity
- P < 0.05
- No pleiotropy
- P = 0.145
Original publication
Visceral adipose tissue and risk of nonalcoholic fatty liver disease: A Mendelian randomization study. Clin Endocrinol (Oxf). Published 10 August 2023. doi:10.
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