Obesity, dyslipidemia, and glucose utilization disorders are the main indicators in the diagnosis of metabolic syndrome. However, there are other markers of damage from oxidative stress, such as the LDL cholesterol (LDL-c) plasma concentration, protein oxidation, lipoperoxidation, and DNA damage. In this study, male Wistar rats (250-270 g) were used. The rats were distributed into eight groups as follows: 1) standard diet and purified water intragastrically (1ml/kg) for seven weeks (N); 2, 3, 4, 5, 6 and 7) hypercholesterolemic diet and 60% fructose for four days (4D);one (1W),two (2W); three (3W), four (4W), five (5W), six (6W) and 7 (7W) weeks respectively and 8) 60% fructose for four weeks (4WF). At the end of treatment, the concentrations of total cholesterol (TC), HDL cholesterol (HDL-c), triglycerides (TGs), and glucose, as well as the alkaline phosphatase activity (ALP), were determined. Moreover, the percentage of cells with DNA migration was determined with a comet assay, and a histopathological study of the hepatic samples was conducted.
The animal model in the current study showed metabolic syndrome (MS) in animals after four weeks with the following well defined markers: decreased HDL-c; increased total cholesterol, LDL-c, atherogenic index, weight gain, and liver weight; hypertension; and defined steatosis leading to an increase in plasma ALP and genotoxic liver damage.