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AIM: To evaluate the effects of ursodeoxycholic acid (UDCA) and/or low-calorie diet (LCD) on a rat model of nonalcoholic steatohepatitis (NASH). METHODS: Fifty-five Sprague-Dawley rats were divided into five groups. The control group (n = 9) was fed with standard rat diet for 12 wk, NASH group (n = 10) was fed with high-fat diet consisted of normal diet, 10% lard oil and 2% cholesterol for 12 wk, UDCA group (n = 10) was fed with high-fat diet supplemented with UDCA at a dose of 25 mg/(kg·d) in drinking water for 12 wk, LCD group (n = 10) was fed with high-fat diet for 10 wk and then LCD for 2 wk, and UDCA+LCD group (n = 15) was fed with high-fat diet for 10 wk, followed by LCD+UDCA for 2 wk. At the end of the experiment, body weight, serum biochemical index, and hepatopathologic changes were examined. RESULTS: Compared with the control group, rats in the NASH group had significantly increased body weight, liver weight, and serum lipid and aminotransferase levels. All rats in the NASH group developed steatohepatitis, as determined by their liver histology. Compared with the NASH group, there were no significant changes in body weight, liver weight, blood biochemical index, the degree of hepatic steatosis, and histological activity index (HAI) score in the UDCA group; however, body and liver weights were significantly decreased, and the degree of steatosis was markedly improved in rats of both the LCD group and the UDCA+LCD group, but significant improvement with regard to serum lipid variables and hepatic inflammatory changes were seen only in rats of the UDCA+LCD group, and not in the LCD group. CONCLUSION: LCD might play a role in the treatment of obesity and hepatic steatosis in rats, but it exerts no significant effect on both serum lipid disorders and hepatic inflammatory changes. UDCA may enhance the therapeutic effects of LCD on steatohepatitis accompanied by obesity and hyperl-ipidemia. However, UDCA alone is not effective in the prevention of steatohepatitis induced by high-fat diet.

AIM: To evaluate the effects of low calorie diet (LCD) on nonalcoholic steatohepatitis (NASH) in rats with obesity and hyperlipidemia. METHODS: 29 Sprague-Dawley (SD) rats were randomly divided into three groups. The animals in control (n = 9) and NASH group (n = 10) were fed on standard rat diet and high fat diet respectively for 12 weeks, ten rats in LCD group were fed on high fat diet for 10 weeks and then low calorie diet for 2 weeks. At the end of the experiment, body weight, abdominal adipose content, liver function, and hepatopathological changes were examined to evaluate the effect of different feeding protocols on the experimental animals. RESULTS: There was no death of animal in the experimental period. All rats in the NASH group developed steatohepatitis according to liver histological findings. Compared with the control group, body weight (423.5 ± 65.2 vs 351.1 ± 43.0 g, P < 0.05), abdominal adipose content (14.25 ± 1.86 vs 9.54 ± 1.43, P < 0.05), liver index (3.784 ± 0.533 vs 2.957 ± 0.301%, P < 0.01), total serum cholesterol (1.60 ± 0.41 vs 1.27 ± 0.17 mmol/L, P < 0.05) and free fatty acids (728.2 ± 178.5 vs 429.2 ± 96.7 mmol/L, P < 0.01), serum alanine aminotransferase (1257.51 ± 671.34 vs 671.34 ± 118.57 nkat/L, P < 0.05) and aspartic aminotransferse (2760.51 ± 998.66 vs 1648.29 ± 414.16 nkat/L, P < 0.01) were significantly increased in the NASH group. Whereas, when rats were fed on LCD protocol, their body weight (329.5 ± 38.4 g, P < 0.01), abdominal adipose content (310.21 ± 1.52 g, P < 0.05), liver index (3.199 ± 0.552%, P < 0.05), and serum alanine aminotransferase (683.03 ± 245.49 nkat/L, P < 0.05) were significantly decreased, and the degree of hepatic steatosis (P < 0.05) was markedly improved compared with those in the NASH group. However, no significant difference was found in serum lipid variables and hepatic inflammatory changes between the two groups. CONCLUSION: LCD might play a role in the prevention and treatment of obesity and hepatic steatosis in SD rats, but it exerts no significant effects on both serum lipid disorders and hepatic inflammatory changes.