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1.南京中医药大学针药结合教育部重点实验室,南京 210023
2.南京中医药大学附属医院, 南京 210029
鲍超,E-mail: drbaochao@163.com
余芝,E-mail: yuzhi@njucm.edu.cn
收稿:2025-07-19,
修回:2025-11-17,
网络首发:2026-05-06,
纸质出版:2026-05-25
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李可,王亚玲,肖文辉,等.迷走神经复合体内的瘦素受体在电针“足三里”抑制肥胖小鼠摄食中的作用[J].针刺研究,2026,51(5):593-602.
LI Ke,WANG Ya-ling,XIAO Wen-hui,et al.Role of leptin receptors in the dorsal vagal complex in the inhibition of food intake in obese mice by electroacupuncture at “Zusanli” (ST36)[J].Acupuncture Research,
李可,王亚玲,肖文辉,等.迷走神经复合体内的瘦素受体在电针“足三里”抑制肥胖小鼠摄食中的作用[J].针刺研究,2026,51(5):593-602. DOI: 10.13702/j.1000-0607.20250778.
LI Ke,WANG Ya-ling,XIAO Wen-hui,et al.Role of leptin receptors in the dorsal vagal complex in the inhibition of food intake in obese mice by electroacupuncture at “Zusanli” (ST36)[J].Acupuncture Research, DOI:10.13702/j.1000⁃0607.20250778.
目的
2
观察背侧迷走神经复合体(DVC)中的瘦素受体(LepR)在电针调控摄食中的作用,探讨电针改善代谢障碍的中枢机制。
方法
2
(1)WT小鼠随机选取10只作为WT正常组,剩余小鼠采用高脂饲料喂养构建食源性肥胖模型,将造模成功的小鼠随机分为WT高脂组、WT电针组,每组10只。WT电针组取“足三里”进行电针干预,20 min/次,每日1次,每周6次,共治疗5周。检测小鼠体质量、摄食量、肝脏及腹股沟白色脂肪组织(iWAT)、附睾白色脂肪组织(eWAT)和棕色脂肪组织(BAT)质量,测定血清胰岛素、瘦素、空腹血糖,进行腹腔葡萄糖耐量实验(IPGTT),检测胃排空率;免疫荧光染色法检测孤束核(NTS)和迷走神经背核(DMV)中LepR阳性神经元与原癌基因c-Fos蛋白(c-Fos)共表达、磷酸化信号转导子和转录激活子3(p-STAT3)表达及DMV中胆碱乙酰转移酶(ChAT)与c-Fos共表达。(2)另设10只LepR敲除小鼠(LepR
-/-
小鼠)随机分为LepR
-/-
正常组和LepR
-/-
电针组,每组5只。LepR
-/-
电针组电针干预方法同前,检测胃排空率。
结果
2
与WT正常组比较,WT高脂组体质量及肝脏、eWAT、iWAT、BAT湿重,血清胰岛素和瘦素,空腹血糖,IPGTT中60、90、120 min的血糖值,糖耐量曲线下面积(AUC)均升高(
P
<
0.01);胃排空率、NTS和DMV中LepR与c-Fos共表达、DMV的p-STAT3表达及ChAT与c-Fos共表达均降低(
P
<
0.01,
P
<
0.05)。与WT高脂组比较,WT电针组摄食量,体质量和肝脏、eWAT、iWAT、BAT湿重,血清瘦素,空腹血糖,IPGTT中60、90、120 min的血糖值,糖耐量AUC均降低(
P
<
0.01);胃排空率、NTS和DMV中LepR与c-Fos共表达、DMV的p-STAT3及ChAT与c-Fos共表达升高(
P
<
0.01,
P
<
0.05)。与WT正常组比较,LepR
-/-
正常组胃排空率升高(
P
<
0.01);与LepR
-/-
正常组对比,LepR
-/-
电针组胃排空率降低(
P
<
0.01)。
结论
2
电针“足三里”可能通过增加肥胖小鼠DVC的LepR,修复迷走中枢信号,促进胃排空以增强饱感,从而抑制摄食。
Objective
2
To observe the role of leptin receptors (LepR) in the dorsal vagal complex (DVC) in electroacupuncture(EA) -mediated regulation of feeding behavior in obese mice, so as to elucidate its central mechanisms underlying improvement of metabolic disorders.
Methods
2
(1) Among wild-type (WT) mice, 10 were randomly selected as the normal group, and the remaining mice were fed with high-fat diet (HFD) to establish a obesity model. The successfully modeled mice were randomly divided into the HFD group and EA group, with 10 mice in each group. The EA group received EA stimulation (2 mA,2 Hz /15 Hz) at bilateral “Zusanli” (ST36) for 20 min, once daily, 6 times per week, for 5 weeks. The body weight, food intake, liver tissue wet weight, inguinal white adipose tissue (iWAT) weight, epididymal white adipose tissue (eWAT) weight, and brown adipose tissue (BAT) weight, and blood glucose levels were measured. The serum insulin and leptin contents were measured using ELISA. The gastric emptying rate was detected using phenol red meal method. Immunofluorescence staining was used to detect the co-expression of LepR-positive neurons and proto-oncogene c-Fos protein (c-Fos), the expression of phosphorylated signal transducer and activator of transcription 3 (p-STAT3), and the co-expression of choline acetyltransferase (ChAT) and c-Fos in the nucleus tractus solitarii (NTS) and dorsal motor nucleus of the vagus nerve (DMV). (2) In addition, 10 leptin receptor knockout (LepR
-/-
) mice were randomly divided into LepR
-/-
normal group and LepR
-/-
EA group, with 5 mice in each group. The LepR
-/-
EA group received the same EA intervention as those described above. Gastric emptying rate was detected as that mentioned above.
Results
2
Compared with the WT normal group, the WT HFD group showed a significant increase in the body weight, liver and adipose (iWAT, eWAT and BAT) wet weight, serum insulin and leptin contents, fasting blood glucose level
, and glucose tolerance area under the curve (AUC, all
P
<
0.01), and a considerable decrease in the gastric empty rate, the number of LepR and c-Fos co-expression neurons in the DMV and NTS, p-STAT3 positive and ChAT and c-Fos co-expression neuron expressions in the DMV (
P
<
0.01,
P
<
0.05). In comparison with the model group, the body weight, food intake, liver and adipose wet weight, serum leptin content, fasting blood glucose, and glucose tolerance AUC were significantly decreased in the EA group (
P
<
0.01), while the gastric empty rate, number of LepR and c-Fos co-expression neurons in the DMV and NTS, p-STAT3 positive and ChAT and c-Fos co-expression neuron expressions in the DMV were notably increased in the EA group (
P
<
0.01,
P
<
0.05). No significant differences were observed in the random blood glucose content and p-STAT3 positive neuron expression in the NTS after modeling and after EA and in the serum level of insulin after EA. (2) Compared with the WT normal group, the LepR
-/-
normal group showed an increase in gastric emptying rate (
P
<
0.01), while in comparison with the LepR
-/-
normal group, the LepR
-/-
EA group exhibited a decrease in gastric emptying rate (
P
<
0.01), suggesting an involvement of LepR in EA-induced enhancement of gastric emptying. There was a positive correlation between the gastric emptying rate and the number of LepR-positive neurons.
Conclusion
2
EA at ST36 can inhibit food intake and promote gastric empty to reduce body weight in obesity mice, which may be associated with its functions in increasing LepR expression in the DVC and restoring vagal central signaling.
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