Objective To explore the role of fat mass and obesity-associated gene (FTO) and its inhibitor rhein in the development of non-alcoholic fatty liver disease (NAFLD).

Methods A NAFLD mouse model was constructed by a high-fat diet and treated with rhein by gavage. To evaluate the success of modeling and the effect of treatment, hematoxylin-eosin (H-E) and oil red staining was used to determine the fat deposition in mouse liver tissues, and Western blot was used to detect the changes of FTO protein expression level in mouse liver tissues.

Results Compared with the general feeding group, the food intake of mice in the high-fat group was significantly lower (P < 0.01), and the body weight of mice in the high-fat+rhein group was significantly lower than that in the high-fat group (P < 0.05). Compared with the high-fat group, the fat vacuoles in the liver cells of mice in the high-fat+rhein group were significantly reduced, the fat deposition in the liver cells of the mice in the high-fat group was significantly more than that in the general feeding group, and the fat deposition in the liver cells of mice fed with rhein was significantly reduced. Compared with the high-fat group, the fat metabolism of mice in the high-fat+rhein group was significantly restored. The expression of FTO protein in the liver tissue of high-fat group was significantly increased, while that in high-fat+Rhein group was significantly decreased.

Conclusions Rhein can reduce the expression of FTO protein in the liver tissue of NAFLD mouse model and has the potential to treat NAFLD.