Over consumption of fructose may lead to obesity and dyslipidemia and cause fructosylation-induced alterations in the structure and function of proteins. The aim of this study was to investigate the role of fructosylated-HSA-AGE in the pathogenesis of fatty liver (NAFLD and NASH) by biochemical, immunological and histological studies. Immunogenicity of fructosylated-HSA-AGE was probed by inducing antibodies in rabbits. Fructosylated-HSA-AGE was found to be highly immunogenic. Furthermore, fructosylated-HSA-AGE caused mild fibrosis with steatosis and portal inflammation of hepatocytes in experimental animals. Liver function test and dyslipidemic parameters in immunized animals were also found to be raised. Ultrasonography, which should form part of the assessment of chronically raised transaminases, shows fatty infiltration. Interestingly, alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, total cholesterol (TC) and triglyceride (TG) profiles confirms USG images of overweight, obese patients. Thus, present study demonstrates that fructosylated-HSA-AGE is hepatotoxic, immunologically active and may cause dyslipidemia.