John Libbey Eurotext

Hépato-Gastro & Oncologie Digestive

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Genetic and epigenetic of non-alcoholic fatty liver disease Volume 24, issue 7, Septembre 2017

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Authors
1 CHU de Nice, Hôpital de l’Archet, service d’hépato-gastroentérologie et de cancérologie digestive, Nice, France
2 INSERM, U1065, C3M, Equipe 8, « Complications hépatiques de l’obésité », Nice, France
3 Université Côte d’Azur, Nice, France

Non-Alcoholic Fatty Liver Disease (NAFLD) is a spectrum of liver diseases that encompass steatosis, Non-Alcoholic Steatohepatitis (NASH) and fibrosis. It is a major public health problem due to its frequency and potential complications (cirrhosis, hepatocellular carcinoma). At present, the monitoring of patients with steatosis or NASH is not fully coded and current treatments are not very effective. Research into the genetics and epigenetics of NAFLD is booming. While genetics studies modifications into the nucleotide sequence of genes, epigenetics studies modifications in the function of a gene that cannot be explained by alterations to the gene sequence. PNPLA3, TM6SF2 and MBOAT7-TMC4 are the 3 main genes for which single nucleotide polymorphisms are associated with steatosis, NASH and hepatic fibrosis, independently of insulin resistance and metabolic syndrome. MicroRNAs (miR), small non-coding RNAs inhibit messenger RNAs and thus regulate gene expression. The expression of some miRs in the liver is modified in NAFLD: miR 122 is decreased and miR 34a is increased. Some miRs are also found in the circulation: for example, miR 122 is increased in the case of NAFLD. Finally, the methylation of target genes is modified in NAFLD resulting in changes in their expression. This is particularly the case for PPAR, a key gene for lipid metabolism. In future, it is likely that substantial genetic and epigenetic data can be obtained for each individual from a simple blood sample allowing personalized monitoring and treatment for NAFLD, as for other diseases.