Abstract

Objective To observe the changes of non-alcoholic fatty liver related indices in diet-induced obesity-resistant rats and diet-induced obesity rats. Methods A total of 140 male Sprague Dawley( SD) rats were randomly divided into normal control group ( n = 20,normal diet for 8 weeks) and model group ( n = 120,high fat diet for 8 weeks). The rats of model group were further divided into 2 groups:O -N ( obesity with non-alcoholic fatty liver) and OR-N ( obesity-resistance with non-alcoholic fatty liver) groups. The rats with body mass higher than mean + 1. 96 folds standard deviation were included in O-N group and those with body mass lower than mean + 1. 0 fold standard deviation were included in OR-N group. The animals with the top 20 weight gains in the O-N group and those with the least 20 weight gains in OR-N group were used in the present study. The general conditions and weight changes of rats were dynamically observed for 8 weeks. Eight rats were sacrificed in each group at the end of the 8th week and the following indices were compared among the three groups,including serum levels of alanine aminotransferase ( ALT) ,total cholesterol ( TC) ,triglyceride( TG) ,high-density lipoprotein ( HDL) ,insulin sensitivity index( ISI) ,leptin,energy utilization and body fat ratio. The pathological changes of liver tissues were observed by H-E staining. Results The weight difference of rats in the O-N group and the OR-N group gradually increased; at the end of the 8th week,the weight of rats in O-N group was significantly higher than those in the OR -N group and the normal control group( P 0. 01). The serum levels of ALT,TG,and leptin were significantly increased in both O-N and OR -N groups ( P 0. 05,P 0. 01). The TC,TG,leptin levels and energy utilization in O-N group were significantly higher than those in OR -N group ( P 0. 05,P 0. 01). The HDL and ISI levels in the O-N group were significantly lower than those in the OR-N and normal control groups ( P 0. 01,P 0. 05). Light microscopy showed a great number of fat vacuoles in the liver cells of O-N and OR-N groups. Conclusion High fat diets can induce SD rat to develop non-alcoholic fatty liver with obesity and obesity-resistance. Increase in serum leptin and ISI may play a role in resisting diet-induced obesity and non-alcoholic fatty liver of rats.

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