RESEARCH NOTE LAB ANIMAL Volume 44, No. 04 | APRIL 2015 135 In recent years, the incidence of diseases such as obesity, insulin resistance, dyslipidemia and type 2 diabetes has increased, owing to both genetic and environmental factors 1,2 . Changes in the nutritional composition of diets, such as increases in refined sugar and saturated fats, as well as lifestyle changes, such as increased sedentary behavior, seem to have a role in the development of these pathologies 3,4 . On the other hand, maintaining blood triglyceride and cholesterol levels within normal ranges is associated with the prevention of diseases such as arteriosclerosis, obesity, cardiovas- cular disease and diabetes. Different nutritional experimental models with metabolic and biochemical characteristics similar to those described in dyslipidemia have been developed. Although the application of these nutritional experi- mental models to humans may be limited, they are extremely useful for research purposes 5,6 . Rabbits fed a high-cholesterol diet have been used to study hyper- lipidemia and atherosclerosis 7 . Similarly, turkeys that consume high-cholesterol foods develop hypercholes- terolemia in rather short periods of time 8 . Rodents are more resistant to high blood cholesterol levels 9 , but some researchers have shown that diet can be used to promote metabolic disturbances in rodents 10,11 . In rats, hypercholesterolemia can be induced by diets high in cholesterol or saturated fat alone or in combination with proteins such as casein 12,13 . Drinks sweetened with sucrose or fructose and diets rich in carbohydrates pro- voke an increase in body weight and hyperlipidemia 14,15 . Changes in body weight and metabolic parameters such as triglyceride, cholesterol, glucose, very-low-density lipoprotein, fibrinogen and total protein have been assessed in such animal models 16–18 , but plasma lipid profiles in animal models fed carbohydrate–rich diets vary among studies. Moreover, several studies have shown that a high-fat, high-sucrose diet can result in metabolic imbalances 19–21 . Hyperlipidemia can also be caused by injections of non-ionic surfactants like poloxamer, which provoke a considerable increase in plasma lipids within 24 h. These substances block the lipoprotein lipase and prevent cholesterol from entering the cell, resulting in an increase in plasma lipoprotein levels and hyperlipidemia 22–24 . They are relatively non- toxic to animals, with LD 50 values reported at 5–34.6 g per kg body weight (ref. 25). Department of Experimental Research, Toxicology Center, Medical College of Villa Clara, Villa Clara, Cuba. Correspondence should be addressed to Y.G.M. (yiselgm@ucm.vcl.sld.cu). Assessment of four experimental models of hyperlipidemia Yisel González Madariaga, MS, María Bofll Cárdenas, PhD, Maibia Tamayo Irsula, MS, Orestes Castillo Alfonso, Bennia Alfonso Cáceres & Emoe Betancourt Morgado, MS Various animal models of hyperlipidemia are used in research. Four rodent hyperlipidemia experimental models are examined in this study: three chronic hyperlipidemia models based on dietary supplementation with lipid or sucrose for 3 months and one acute hyperlipidemia model based on administration of the nonionic surfactant poloxamer. Neither lipid supplementation nor sucrose supplementation in Wistar rats was effective for establishing hyperlipidemia. Combining both lipid and sucrose supplementation in BALB/c mice induced hypercholesterolemia, as reflected in a considerable increase in blood cholesterol concentration, but did not produce an increase in blood triglyceride concentration. Poloxamer administration in C57BL/J6 mice produced increases in blood cholesterol and triglyceride concentrations. The authors conclude that supplementation of both lipid and sucrose in BALB/c mice was the most effective method for developing chronic hypercholesterolemia. © 2015 Macmillan Publishers Limited. All rights reserved