Lipids & metabolic liver disease
Mendelian randomisation reveals Sodium-glucose Cotransporter-1 inhibition's potential in reducing Non-Alcoholic Fatty Liver Disease risk
Authors' conclusion
Overall, genetically proxied SGLT-1i is associated with improved liver health, this may be underpinned by SGLT-1-specific mechanisms.
Study context
- Population
- Non-alcoholic fatty liver disease (NAFLD) cases and controls; exposure instrument from HbA1c genome-wide association study1,483 cases · 17,781 controls · HbA1c genome-wide association study 344,182
- Comparison
- Genetically proxied SGLT-1 inhibition
- Outcome
- NAFLD risk
Methodological detailsgenetic proxy: missense variant rs17683430 in SLC5A1, colocalisation
- Genetic proxy: missense variant rs17683430 in SLC5A1
- Colocalisation
Main finding
As reported in the abstract
OR per 1 mmol/mol HbA1c reduction via genetically proxied SGLT-1i
0.36
95% CI 0.15, 0.87P = .023
Further findings
Liver enzymes (ALT, AST, GGT)
- Genetically proxied SGLT-1i associated with reductions in alanine transaminase, aspartate transaminase and gamma-glutamyl transferase
Genetically proxied HbA1c, not specifically via SGLT-1i, and NAFLD risk
- Not associated with NAFLD risk
Colocalisation
- No evidence of genetic confounding
Original publication
Mendelian randomisation reveals Sodium-glucose Cotransporter-1 inhibition's potential in reducing Non-Alcoholic Fatty Liver Disease risk. Eur J Endocrinol. Published 21 June 2023. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →