[Mechanism of Electropuncture for Reducing Diet-induced Obesity Rat Weight through Hypothala- mus TSC1 -mTOR Signal Pathway].

To explore the mechanism of electropuncture (EA) for reducing diet-induced obesity (DIO) rat weight through tuberous sclerosis complex 1 (TSC1 )-mammalian target of rapa- mycin (mTOR) signal pathway in hypothalamus.Forty male SD rats were randomly divided into the model group (n =30) and the normal control group (n =10). DIO rat model was prepared by high fat forage for 12 successive weeks. Successfully modeled 19 rats were further randomly divided into the model group (n =9) and the EA group (n =10). EA at Tianshu (ST25) , Sanyinjiao (SP6) , Zhongwan ( RN12) , Zusanli (ST36) was performed in the EA group, 5 successive days per week with a 2-day rest, 4 weeks in total. No intervention was given to rats in the model group and the normal control group. Body weight was observed in all rats. Methylation of TSC1 promotor was detected by bisulfite sequencing method. mRNA expression of mTOR in hypothalamus was detected by RT-PCR.After EA treatment body weight in the EA group were obviously reduced (P <0. 05). Compared with the normal control group, body weight was not statistically different between the model group and the EA group after treatment (P> 0. 05). Methylation rate of TSC1 promotor was higher in model group (94. 0% ±4. 5%) than in the normal control group (87. 0% ±3. 6%) and the EA group (87. 4% ±3. 9%) (P <0. 05). Expression of mTOR in the model group (1. 84 ±0. 51) was higher than that in the normal control group (1. 02 ±0. 22) and the EA group (1. 46 ±0. 29) (P <0. 05).EA could lower DIO rats' body weight by down-regulating methylation rate of TSC1 promotor and regulating expression of mTOR in hypothalamus.