Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver damage, and is characterized by excess fat accumulating in the liver due to causes other than alcohol use. Researchers have identified a gene which may be associated with the initiation of NAFLD.
Sequencing biochemical molecules obtained from liver biopsies of 30 female candidates for gastric bypass surgery, the research team observed a significant suppression of a protein called FOX03 in damaged livers, compared to those without liver damage. These findings suggest a potential role for this gene in the initiation of liver disease.
The study’s senior author Johanna DiStefano from Translational Genomics Research Institute (Tgen) in Arizona, US, said, “To our knowledge, this is the first study to apply a high-throughput sequencing approach to the investigation of liver microRNAs (miRNAs) in NAFLD-related liver damage.”
The miRNAs, RNA molecules that regulate gene expression, were obtained from liver biopsies of 30 female candidates for gastric bypass surgery- 15 with, and 15 without, NAFLD liver damage. Using the most advanced technology to refine the data, the research team identified several potential gene targets associated with NAFLD-related liver damage. Specifically, the researchers found that a particular miRNA called miR-182 produced a strong association with a protein called FOX03.
Study’s lead author Fatjon Leti, research associate at Tgen said, “Because of the known role of miR-182 in mechanisms related to liver cancer, we sought to investigate this miRNA in NAFLD-related liver damage by looking at relevant target genes. We found that levels of FOX03, which has been implicated in liver metabolism, to be significantly decreased.”
The findings appeared in Translational Research.