首页|期刊导航|中国实验动物学报|穴位埋线通过纠正糖脂代谢紊乱和诱导内脏白色脂肪褐变改善大鼠腹型肥胖

穴位埋线通过纠正糖脂代谢紊乱和诱导内脏白色脂肪褐变改善大鼠腹型肥胖OA

Acupoint catgut embedding improves abdominal obesity by regulating glucose-lipid metabolism and inducing visceral white adipose tissue browning

中文摘要英文摘要

目的 观察穴位埋线对腹型肥胖(abdominal obesity,AO)大鼠肥胖程度、糖脂代谢和白色脂肪褐变的影响,探索其减重机制.方法 60只SD大鼠随机分为对照组(10只)和AO组(50只),高脂饮食建立AO模型.将造模成功的30只AO大鼠随机分为模型组、穴位埋线组和假埋线组(各10只).穴位埋线组在麻醉下于单穴点"中脘、关元"以及双穴点"天枢、大横、带脉、丰隆、脾俞"行埋线治疗,1周1次,共8次;假埋线组不置入线体;对照组和模型组仅麻醉.检测各组体质量、腹围、Lee's指数、摄食量以及腹股沟白色脂肪(iWAT)质量、附睾白色脂肪(eWAT)质量、血清脂质(TC、TG、LDL-C和HDL-C)和胰岛素相关指标(FBG、FINS和HOMA-IR),Western Blot 和 qPCR 测定 eWAT 中白色脂肪褐变分子(UCP1、PGC-1α、PPARγ 和PRDM16)蛋白和mRNA表达.结果 与对照组相比,模型组肥胖指标、脂肪组织质量(iWAT和eWAT)、FBG、FINS、HOMA-IR、TC、LDL-C 升高,HDL-C 下降,褐变分子表达下调(P<0.05 或 P<0.01 或 P<0.001).与模型组相比,穴位埋线组肥胖指标、脂肪组织质量(iWAT和eWAT)下降,糖脂代谢指标改善,褐变分子上调(P<0.05或P<0.01或P<0.001);假埋线组与模型组上述指标差异不显著(P>0.05).与假埋线组相比,穴位埋线组肥胖指标、iWAT质量下降,糖脂代谢改善,褐变分子表达增加(P<0.05或P<0.01或P<0.001),而eWAT质量无统计学意义(P>0.05).相关性分析显示,eWAT中褐变分子表达水平与糖脂代谢指标的改善具有显著相关性.结论 穴位埋线可改善AO大鼠的肥胖状态,其机制可能与调节糖脂代谢、促进内脏白色脂肪褐变有关.

Objective To investigate the effects of acupoint catgut embedding(ACE)on obesity,glucose-lipid metabolism,and white adipose tissue(WAT)browning in rats with abdominal obesity(AO),and to explore its potential weight-loss mechanisms.Methods Sixty SD rats were randomly assigned to control(n=10)and modeling groups(n=50).AO models were established through high-fat diet feeding.Thirty successfully modeled rats were randomly divided into model group,ACE,and sham acupoint catgut embedding(SACE)groups(n=10 each).The ACE group received treatment under anesthesia at the single acupoints"Zhongwan and Guanyuan",and bilateral acupoints"Tianshu,Daheng,Daimai,Fenglong and Pishu"once weekly for 8 weeks.The procedure was performed without embedding the thread in the SACE group;the control and model groups received anesthesia only.Body mass,abdominal circumference,Lee's index,food intake,inguinal WAT(iWAT)and epididymal WAT(eWAT)mass,serum lipids(total cholesterol(TC),triglycerides(TG),low-density lipoprotein cholesterol(LDL-C),high-density lipoprotein cholesterol(HDL-C)),and insulin-related indices(fasting blood glucose(FBG),fasting insulin(FINS),homeostasis model assessment of insulin resistance(HOMA-IR))were measured.Protein and mRNA expression levels of browning-related markers in eWAT,including uncoupling protein 1(UCP1),peroxisome proliferator-activated receptor gamma coactivator-1 α(PGC-1α),peroxisome proliferator-activated receptor γ(PPARγ),and PR domain containing 16(PRDM16),were assessed using Western Blot and qPCR.Results Compared with the control group,the model group showed increased obesity indices,iWAT and eWAT mass,FBG,FINS,HOMA-IR,TC,and LDL-C,decreased HDL-C,and downregulation of browning-related molecules(P<0.05 or P<0.01 or P<0.001).Compared with the model group,the ACE group showed reductions in obesity indices and WAT mass(iWAT and eWAT),improvements in glucose-lipid metabolism,and upregulation of browning molecules(P<0.05 or P<0.01 or P<0.001);no significant changes were observed in the SACE group versus the model group(P>0.05).Compared with the SACE group,the ACE group exhibited reduced obesity indices and iWAT mass,improved lipid and insulin-related parameters,and increased expression of browning-related molecules(P<0.05 or P<0.01 or P<0.001),while eWAT mass did not differ significantly(P>0.05).Correlation analysis further demonstrated that browning-related marker expression in eWAT was significantly associated with improvements in glucose-lipid metabolic parameters.Conclusions Acupoint catgut embedding reduces AO in rats,possibly through regulating glucose-lipid metabolism and promoting visceral WAT browning.

黎明;朱敏;晏明熙;全菲;崔瑾

贵州中医药大学针灸推拿学院,贵州 550025成都市第七人民医院/成都医学院附属肿瘤医院中医科,成都 610213贵州中医药大学针灸推拿学院,贵州 550025贵州中医药大学针灸推拿学院,贵州 550025||贵州中医药大学第一附属医院针灸科,贵州 550001贵州中医药大学针灸推拿学院,贵州 550025||贵州中医药大学第一附属医院针灸科,贵州 550001

生物科学

穴位埋线腹型肥胖糖脂代谢脂肪组织白色脂肪褐变

acupoint catgut embeddingabdominal obesityglucose-lipid metabolismadipose tissuewhite adipose tissue browning

《中国实验动物学报》 2026 (8)

1176-1188,13

国家重点研发项目(3416-416230019).Funded by National Key Research and Development Project(3416-416230019).

10.3969/j.issn.1005-4847.2026.08.008

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