Objective To Investigate the pathogenetic mechanism of nonalcoholic fatty liver disease ( NAFLD) in gerbils，the changes in the lipid metabolism，liver function and antioxidation in its development caused by high fat diet．Methods One hundred and twenty gerbils were divided randomly into 2 groups: the model group fed with high fat diet and control group fed with normal diet． Ten gerbils were killed at 1，2，4，6，8 and 16 weeks after the start of diet，respectively． The pathological changes of the liver were examined，and the liver index，serum CHO，TG，LDL-c，HDL-c，GOP，GPT，the liver SOD，GSH-PX，CAT，FFA were determined． Results In the model group，simple fatty liver was observed at 2 weeks，mild inflammation in the hepatic portal areas at 6 weeks，focal perisinosodal fibrosis/ pericellular fibrosis of acini band at 8 weeks，and moderate liver fibrosis at 16 weeks after the start of diet． CHO，HDL-C，LDL-C and FAA were obviously elevated ( P ﹤ 0. 05，P ﹤ 0. 01) at 1，2，4，6，8，16 weeks，TG was raised at 1，2，4 weeks( P ﹤ 0. 05，P ﹤ 0. 01 ) ，GOT and GPT were Significantly increased after 16 weeks ( P ﹤ 0. 01 ) ，GSH-PX、CAT and SOD were Significantly decreased after 8 weeks( P ﹤ 0. 05，P ﹤ 0. 01 ) ． Conclusions Gerbil models of simple fatty liver can be developed at 2 weeks after high fat diet feeding，and moderate liver fibrosis after 16 weeks． Lipid metabolic disorders and oxidative stress play different roles in the development of nonalcoholic fatty liver disease．