[Electroacupuncture promotes browning of white adipose tissue by regulating mTOR/SREBP1 signaling pathway in obese mice].
پخش حرفهای فارسی و انگلیسی
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چکیده اصلی
OBJECTIVE: To investigate the regulatory effect of electroacupuncture (EA) at "Zusanli" (ST36) and "Tianshu"(ST25) on the mammalian target of rapamycin (mTOR)/sterol regulatory element-binding protein 1 (SREBP1) signaling pathway in obese mice, and to analyze its mechanism in promoting the browning of white adipose tissue for the prevention and treatment of obesity. METHODS: Among 38 male C57BL/6J mice of SPF grade, 8 mice were randomly selected as the normal group, and the remaining 30 mice were fed with high-fat diet to establish obesity model. Sixteen successfully modeled mice were randomly divided into a model group and an EA group, 8 mice in each group. In the EA group, EA was applied at bilateral "Zusanli" (ST36) and "Tianshu" (ST25), 30 min a time, once daily, 5 times a week, for 4 consecutive weeks. Body mass was measured before and after intervention, and Lee's index was calculated. After intervention, fasting blood glucose,insulin, and serum lipid profile indexes (total cholesterol [TC], triglyceride [TG], low-density lipoprotein cholesterol [LDL-C]and high-density lipoprotein cholesterol [HDL-C]) were detected by ELISA, and the insulin resistance index was calculated;abdominal adipose tissue mass was measured, and the morphology of abdominal adipose tissue was observed by HE staining;the mRNA expression of mTOR, SREBP1, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α),uncoupling protein 1 (UCP1), PR domain-containing protein 16 (PRDM16) and cell death-inducing DNA fragmentation factor-α-like effector A (Cidea) in abdominal adipose tissue was detected by real-time fluorescent quantitative PCR, the protein expression of mTOR, SREBP1, PGC-1α, UCP1, PRDM16 and Cidea in abdominal adipose tissue was detected by Western blot. RESULTS: Compared with the normal group, in the model group, the body mass and abdominal adipose tissue mass were increased (P<0.01); the Lee's index, fasting blood glucose, insulin level and insulin resistance index were increased (P<0.01); the serum levels of TC, TG and LDL-C were increased (P<0.01), and the serum HDL-C level was decreased (P<0.01); the adipocyte diameter in abdominal adipose tissue was enlarged; the mRNA and protein expression of mTOR and SREBP1 was increased (P<0.01), and the mRNA and protein expression of PGC-1α, UCP1, PRDM16 and Cidea in abdominal adipose tissue was decreased (P<0.01). Compared with the model group, in the EA group, the body mass and abdominal adipose tissue mass were reduced (P<0.01); the Lee's index, fasting blood glucose, insulin level and insulin resistance index were decreased (P<0.01); the serum levels of TC, TG and LDL-C were decreased (P<0.01), and the serum HDL-C level was increased (P<0.01); the adipocyte diameter in abdominal adipose tissue was reduced; the mRNA and protein expression of mTOR and SREBP1 was decreased (P<0.05), and the mRNA and protein expression of PGC-1α,UCP1, PRDM16 and Cidea in abdominal adipose tissue was increased (P<0.01). CONCLUSION: EA at "Zusanli" (ST36) and"Tianshu" (ST25) can alleviate obesity and regulate glycolipid metabolic disorders in mice. The mechanism may be related to inhibiting the mTOR/SREBP1 signaling pathway, up-regulating the expression of PGC-1α, UCP1, PRDM16 and Cidea, and promoting the browning of white adipose tissue.
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