Reevaluating the causal link between liver fat and hyperglycaemia
Authors' conclusion
The absence of a causal relationship between hepatic steatosis and glycaemic traits suggests that hyperglycaemia in metabolic dysfunction-associated steatotic liver disease may involve additional mechanisms beyond liver fat accumulation.
Study context
- Population
- Genome-wide association study (GWAS) data from 37,358 individuals (Mendelian randomisation (MR)); 13 RCTs of liver fat-targeted drugs13 RCTs of liver fat-targeted drugs 2,482
- Participants
- 37,358 GWAS individuals
- Comparison
- Genetically predicted liver fat and glycaemic traits; liver fat-targeted drugs vs controls
- Outcome
- Causal effect of liver fat on fasting glucose, HbA1c, postprandial glucose, fasting insulin and HOMA-IR
Methodological detailsGWAS data, meta-regression
- GWAS data
- Meta-regression
Pooled result
As reported in the abstract
Causal effect of liver fat content on glycaemic traits (MR)
- Fasting glucose level: β = −0.006; p = 0.827
- HbA1c level: β = −0.009; p = 0.366
- Postprandial glucose level: β = −0.063; p = 0.257
- Fasting insulin level: β = 0.010; p = 0.691
- Homeostatic model assessment of insulin resistance (HOMA-IR): β = 0.001; p = 0.965
- No causal effect of liver fat content on glycaemic traits
Further pooled results
| Outcome | SMD (95% CI) | |
|---|---|---|
| Change in fasting blood glucose (meta-analysis, 13 RCTs, n = 2482) | −0.09 (−0.18 to 0.01) | |
| Change in HbA1c (meta-analysis, 13 RCTs, n = 2482) | −0.02 (−0.12 to 0.07) | |
| −0.2−0.100.1Difference (linear scale) |
Meta-regression: liver fat reduction vs changes in fasting blood glucose or HbA1c
- No statistically significant linear relationship between liver fat reduction and changes in fasting blood glucose or HbA1c
Original publication
Reevaluating the causal link between liver fat and hyperglycaemia. Diabetes Obes Metab. Published 6 October 2025. doi:10.
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