Genetic variants and diet both influence risk of hepatic steatosis, inflammation/fibrosis, and hepatic decompensation; however, how gene-diet interactions influence these outcomes has previously not been comprehensively characterized. We investigated this topic in the community-based UK Biobank and found that genetic risk and dietary quality interacted to influence hepatic steatosis and inflammation/fibrosis on liver MRI, so that the effects of diet were greater in people at elevated genetic risk. These results are relevant for patients and medical providers because they show that genetic risk is not fixed (i.e. modifiable factors can mitigate or exacerbate this risk) and realistic dietary changes may result in meaningful improvement in liver steatosis and inflammation/fibrosis. As genotyping becomes more routinely used in clinical practice, patients identified to be at high baseline genetic risk may benefit even more from intensive dietary counseling than those at lower risk, though future prospective studies are required.
Keyphrases
- genome wide
- end stage renal disease
- oxidative stress
- clinical practice
- physical activity
- chronic kidney disease
- magnetic resonance imaging
- newly diagnosed
- healthcare
- weight loss
- adipose tissue
- prognostic factors
- gene expression
- dna methylation
- peritoneal dialysis
- transcription factor
- cross sectional
- human immunodeficiency virus
- metabolic syndrome
- mass spectrometry