| Objective: To observe effects of calorie restriction (CR) and high energy including high glucose (HG) and high lipid (HP) on the expression of sirtuin family in HepG2 cells and to provide insights for further studies on its roles in related metabolic diseases.Methods: Total mRNA and proteins was extracted when the cells was cultured for 24h in low glucose, high glucose or high lipid media. RT-PCR was used to detect the mRNA transcription level of sirtuins family in HepG2 cells cultured in low glucose, high glucose or high palmitate. Western blot was used to detect the protein level of sirtuins family in HepG2 cells.Results:1. RT-PCR showed that, on the level of mRNA, CR significantly up-regulated the expression of SIRT1, SIRT5 and SIRT7, while down-regulated the expression of SIRT3 and SIRT4, no significantly influence on SIRT6 in HepG2 cells compared with HG culture. On the level of mRNA, HP significantly up-regulated the expression of SIRT1, SIRT5, SIRT6 and SIRT7, while no significant influence on SIRT6 in HepG2 cells compared with HG culture. On the level of mRNA, HP significantly up-regulated the expression of SIRT1, SIRT4 and SIRT7, while down-regulated the expression of SIRT5, no significant influence on SIRT3 and SIRT6 in HepG2 cells compared with CR culture. 2. Western blot showed that, on the level of protein, CR significantly up-regulated the expression of SIRT1 and SIRT7, while there was no significant influence on SIRT2 in HepG2 cells compared with HG culture. On the level of protein, HP significantly up-regulated the expression of SIRT1 and SIRT7, while there was no significant influence on SIRT2 in HepG2 cells compared with HG and CR cultures.Conclusion: The effects of CR and HP on the expression of sirtuins family are different compared with HG. These results suggest that sirtuins family may be co-involved in the regulation of CR on the energy metabolization including SIRT1. Besides, sirtuins family may be involved in the regulation of glycose and lipid metabolism in the liver, thus affecting the formation of fatty liver. |