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High energy-intake is a major factor revolved in type 2 diabetes. A number of animal models have been adopted for studying the type 2 diabetes, but they differ greatly from human type 2 diabetes. The objectives of the present study are to set tip a suitable animal model, which is similar to the human type 2 diabetes, and then to understand possible molecular mechanisms underlying type 2 diabetes. Twenty five-week-old Wistar male rats were randomized into four groups. One group was fed with basal diet (BD) whereas the others consumed high-energy diet (HD) of 20% sucrose and 10% lard. Four weeks later, BD and one of HD were sampled. Other groups continued to consume HD, but one of them was treated by one injection of streptozotocin (STZ) 130mg/kg body weight). After another four weeks, all were sacrificed. Changes in body weight were recorded, and levels of glucose. TG, TC, LDL in serum were analyzed by standard methods. Moreover, expressions of genes related to energy metabolism in liver, muscle and fat were measured by real-time RT-PCR. HD had no notable differentiation with BD on bodyweight and serum indices, but it altered gene expressions in a tissue-specific manner. Two receptors of adiponeefin, lepfin, PPARγ, UCP2 mRNA levels in fat were up regulated, whereas most of them were down regulated in liver. STZ treatment induced symptoms of diabetes, and the gene expression mentioned above exhibited changes in both tissue-and gene-specific manners. The results suggest that a combination of low dose STZ and high-energy intake can effectively induce type 2 diabetes by altering the related gene expressions in major metabolic tissues. [ABSTRACT FROM AUTHOR]