Iron depletion attenuates steatosis in a mouse model of non-alcoholic fatty liver disease: Role of iron-dependent pathways

Iron has been proposed as influencing the progression of liver disease in subjects with non-alcoholic fatty (NAFLD). We have previously shown that, Hfe−/− mouse model hemochromatosis, feeding a high-calorie diet (HCD) leads to increased injury. In this study we investigated whether an iron deficient/HCD mice influenced development NAFLD. Liver histology was assessed fed standard iron-containing or iron-deficient plus minus HCD. Hepatic concentration, serum transferrin saturation and free acid were measured. Expression genes implicated regulation determined by quantitative real-time PCR (qRT-PCR). Standard iron/HCD-fed developed severe steatosis whereas NAS score reduced Mice HCD had lower weights, decreased ferroportin hepcidin gene expression than HCD-fed mice. Serum non-esterified acids compared analysis indicated that involved fatty-acid binding mTOR pathways regulated depletion. Our results indicate decreasing intake attenuates resulting from high calorie diet. These also suggest human studies agents modify balance patients NAFLD should be revisited.