To explore the correlation between hepatic fat and fibrosis and the possible causative mechanism. 40 Wistar rats were randomized into 4 groups i.e. low fat diet (group I), high fat diet (group II), low fat diet plus ethanol (group III), high fat diet plus ethanol (group IV). Rats were sacrificed at 3 and 6 months after experiment. Triglyceride (TG), malonaldehyde (MDA) and hydroproline (Hyp) content in the liver were measured with biochemical analysis. The degree of steatosis and fibrosis and the amount of alpha-smooth muscle actin (alpha-SMA) positive cells in the liver were determined by HE, van Giesson and immunohistochemical ABC stain, respectively.
Results: Steatosis was observed in most of the group II, III, IV animals including those sacrificed at 3 months after experiment, but increased amount of alpha-SMA positive cells and hepatic fibrosis was only shown in group III and IV. As compared with group I, hepatic TG content was increased significantly in the group II, III, IV animals, and hepatic MDA and Hyp content were increased significantly in the group III, IV animals. Moreover, changes of these biochemical and histological indexes in group IV were the most outstanding. There was no significant correlation between hepatic TG content and amount of alpha-SMA positive cells in group II, III, IV and no correlation between hepatic TG and Hyp content in group II, IV, and there was significant correlation between hepatic MDA content and Hyp content and the number of alpha-SMA positive cells in group III, IV.
Conclusions: There is no direct relationship between steatosis and initiation of lipocyte activation and resulting fibrogenesis, but hepatic fat per se may promote the initiation and development of hepatic fibrosis induced by the injurious factors of increasing lipid peroxidation.