电针调控mTOR/SREBP1信号通路促进肥胖小鼠白色脂肪棕色化的机制研究

张英溶; 黄伟; 张艳佶; 夏郡妮; 王艺霏; 张子怡; 廖璐璐; 程好; 饶映月; 周仲瑜

doi:10.13703/j.0255-2930.20250221-k0001

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电针调控mTOR/SREBP1信号通路促进肥胖小鼠白色脂肪棕色化的机制研究

机制探讨 | 更新时间：2026-09-15

- 电针调控mTOR/SREBP1信号通路促进肥胖小鼠白色脂肪棕色化的机制研究
- Electroacupuncture promotes browning of white adipose tissue by regulating mTOR/SREBP1 signaling pathway in obese mice
- 中国针灸 2026年46卷第9期页码：1482-1490
- 作者机构：
  
  湖北省中医院针灸诊疗中心，武汉　430061
  湖北中医药大学附属医院针灸诊疗中心，武汉　430061
  湖北省中医药研究院，武汉　430061
  湖北时珍实验室，武汉　430061
  湖北中医药大学针灸骨伤学院
  中医肝肾研究及应用湖北省重点实验室，武汉　430061
- 作者简介：
  
  ✉周仲瑜，二级教授、主任医师。E-mail：2209447940@qq.com
- 基金信息：
  
  武汉市科技局知识创新专项项目(2023020201010172);湖北中医药大学"双一流"建设重点类专项科研项目(2023ZZXT005);湖北省第二届医学领军人才工程培养对象暨湖北名医工作室项目(鄂卫通〔2019〕47号);国家中医药管理局第七批全国老中医药专家学术经验工作继承项目(国中医药办人教函〔2021〕272号);国家中医药管理局全国名老中医（王华教授）传承工作室(QZ202301);国家自然科学基金资助项目(81674081);湖北省科技计划项目(2025BCB024)
- DOI：10.13703/j.0255-2930.20250221-k0001
  中图分类号：
- 收稿：2025-02-21，
  
  网络首发：2026-07-23，
  
  纸质出版：2026-09-12
- 稿件说明：
移动端阅览
张英溶, 黄伟, 张艳佶, 等. 电针调控mTOR/SREBP1信号通路促进肥胖小鼠白色脂肪棕色化的机制研究[J]. 中国针灸, 2026,46(9):1482-1490.

ZHANG Yingrong, HUANG Wei, ZHANG Yanji, et al. Electroacupuncture promotes browning of white adipose tissue by regulating mTOR/SREBP1 signaling pathway in obese mice[J]. Chinese Acupuncture & Moxibustion, 2026, 46(9): 1482-1490.
张英溶, 黄伟, 张艳佶, 等. 电针调控mTOR/SREBP1信号通路促进肥胖小鼠白色脂肪棕色化的机制研究[J]. 中国针灸, 2026,46(9):1482-1490. DOI： 10.13703/j.0255-2930.20250221-k0001.

ZHANG Yingrong, HUANG Wei, ZHANG Yanji, et al. Electroacupuncture promotes browning of white adipose tissue by regulating mTOR/SREBP1 signaling pathway in obese mice[J]. Chinese Acupuncture & Moxibustion, 2026, 46(9): 1482-1490. DOI： 10.13703/j.0255-2930.20250221-k0001.

摘要

目的：

探讨电针“足三里”“天枢”对肥胖小鼠哺乳动物雷帕霉素靶蛋白（mTOR）/固醇调节元件结合蛋白1（SREBP1）信号通路的调控作用，分析其促进白色脂肪棕色化防治肥胖症的作用机制。

方法：

从38只SPF级雄性C57BL/6J小鼠中随机选取8只作为正常组，其余30只小鼠采用高脂饲料喂养建立肥胖模型，将16只造模成功的小鼠随机分为模型组和电针组，每组8只。电针组取双侧“足三里”“天枢”行电针干预，每次30 min，每日1次，每周5次，持续4周。测量各组小鼠干预前后体质量并计算Lee′s指数。干预后，采用ELISA法检测各组小鼠空腹血糖、胰岛素及血脂四项[总胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白胆固醇（LDL-C）及高密度脂蛋白胆固醇（HDL-C）]水平，并计算胰岛素抵抗指数；称量各组小鼠腹部脂肪组织质量，采用HE染色法观察各组小鼠腹部脂肪组织形态；实时荧光定量PCR法检测各组小鼠腹部脂肪组织mTOR、SREBP1、过氧化物酶体增殖物激活受体γ共激活因子-1α（PGC-1α）、解偶联蛋白1（UCP1）、PR结构域蛋白16（PRDM16）、诱导细胞死亡的DNA片段化因子α样效应因子（Cidea）mRNA表达；Western blot法检测各组小鼠腹部脂肪组织mTOR、SREBP1、PGC-1α、UCP1、PRDM16、Cidea蛋白表达。

结果：

与正常组比较，模型组小鼠体质量及腹部脂肪组织质量增加（

0.01）；Lee′s指数、空腹血糖、胰岛素水平及胰岛素抵抗指数升高（

0.01）；血清TC、TG、LDL-C水平升高（

0.01），HDL-C水平降低（

0.01）；腹部脂肪组织脂肪细胞直径增大；腹部脂肪组织mTOR、SREBP1的mRNA和蛋白表达升高（

0.01），PGC-1α、UCP1、PRDM16、Cidea的mRNA和蛋白表达降低（

0.01）。与模型组比较，电针组小鼠体质量及腹部脂肪组织质量减少（

0.01）；Lee′s指数、空腹血糖、胰岛素水平及胰岛素抵抗指数降低（

0.01）；血清TC、TG、LDL-C水平降低（

0.01），HDL-C水平升高（

0.01）；腹部脂肪组织脂肪细胞直径减小；腹部脂肪组织mTOR、SREBP1的mRNA和蛋白表达降低（

0.05），PGC-1α、UCP1、PRDM16、Cidea的mRNA和蛋白表达升高（

0.01）。

结论：

电针“足三里”“天枢”可减轻小鼠肥胖，调节糖脂代谢紊乱，其机制可能与抑制mTOR/SREBP1信号通路，上调PGC-1α、UCP1、PRDM16及Cidea表达，促进白色脂肪棕色化有关。

Abstract

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 (

0.01); the Lee's index

fasting blood glucose

insulin level and insulin resistance index were increased (

0.01); the serum levels of TC

TG and LDL-C were increased (

0.01)

and the serum HDL-C level was decreased (

0.01); the adipocyte diameter in abdominal adipose tiss

ue was enlarged; the mRNA and protein expression of mTOR and SREBP1 was increased (

0.01)

and the mRNA and protein expression of PGC-1α

UCP1

PRDM16 and Cidea in abdominal adipose tissue was decreased (

0.01). Compared with the model group

in the EA group

the body mass and abdominal adipose tissue mass were reduced (

0.01); the Lee's index

fasting blood glucose

insulin level and insulin resistance index were decreased (

0.01); the serum levels of TC

TG and LDL-C were decreased (

0.01)

and the serum HDL-C level was increased (

0.01); the adipocyte diameter in abdominal adipose tissue was reduced; the mRNA and protein expression of mTOR and SREBP1 was decreased (

0.05)

and the mRNA and protein expression of PGC-1α

UCP1

PRDM16 and Cidea in abdominal adipose tissue was increased (

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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