A diet high in sucrose, which is a common food constituent, induces obesity and non- alcoholic fatty liver (NFLD) caused by high caloric intake; however, it is important to investigate those sequential changes in the hepatic parenchyma related to sugar consumption which are associated to obesity and dyslipidemia. We analyzed the effects of long-term sucrose intake on fatty liver development, by the administration of 30% sucrose in drinking water in healthy Wistar rats during 30 weeks. Serum variables, body fat index, caloric intake and microscopic examination of liver tissue were monitored. In the first week, grade 1 steatosis was observed with ballooned hepatocytes, with a caloric intake of 125 ± 1.90 kcal / day / 100 g of body weight; together with a gain of 71% in abdominal fat with respect to the control group and dyslipidemia. During the 10 to 20 weeks period, steatosis grade 2 with noticeable inflammation (steatohepatitis), polymorphic cells and ballooned hepatocytes were evident. After 10 weeks, the caloric intake was 72.9 ± 5.99 kcal / day / 100 g of body weight with 199% of gain in abdominal fat in SUC groups with respect control group (p < 0.01) and moderate dyslipidemia; while after 20 weeks, the caloric intake was 61.6 ± 4.65 kcal / day / 100 g of body weight with 208% of gain in abdominal fat and also moderate dyslipidemia. After 30 weeks steatosis grade 3 with marked inflammation (steatohepatitis), periportal fibrosis, globose and fat-filled hepatocytes were observed, with a caloric intake of 52.3 ± 3.05 kcal / day / 100 g of body weight and 232% of gain in abdominal fat that was related to severe dyslipidemia. In conclusion, the sequential changes in the development of NAFLD were associated with the ingestion of sucrose and obesity since the first week of administration.
Keywords: Obesity; fatty liver; metabolic syndrome; steatohepatitis; steatosis; sucrose.