[1]周松兰,杨晓瑞,熊清,等.Nesfatin-1激活PPARγ信号通路调节脂代谢改善大鼠肥胖症实验研究[J].陕西医学杂志,2025,54(6):748-753.[doi:DOI:10.3969/j.issn.1000-7377.2025.06.005]
　ZHOU Songlan,YANG Xiaorui,XIONG Qing,et al.Nesfatin-1 regulates lipid metabolism and improves obesity in rats by activating PPARγ signaling pathway[J].,2025,54(6):748-753.[doi:DOI:10.3969/j.issn.1000-7377.2025.06.005]
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Nesfatin-1激活PPARγ信号通路调节脂代谢改善大鼠肥胖症实验研究

《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
54
期数:
2025年6期
页码:
748-753
栏目:
基础研究
出版日期:
2025-06-05

文章信息/Info

Title:
Nesfatin-1 regulates lipid metabolism and improves obesity in rats by activating PPARγ signaling pathway
作者:
周松兰; 杨晓瑞; 熊清; 黄洁杰; 李春; 周琼; 梅聪; 彭葆坤; 王毅鹏
（昆明市延安医院内分泌科，云南 昆明 650051）
Author(s):
ZHOU Songlan; YANG Xiaorui; XIONG Qing; HUANG Jiejie; LI Chun; ZHOU Qiong; MEI Cong; PENG Baokun; WANG Yipeng
(Department of Endocrinology,Yan’an Hospital of Kunming City,Kunming 650051,China)
关键词:
肥胖症; 摄食抑制因子1; 过氧化物酶体增殖物激活受体γ; 脂代谢; 血脂
Keywords:
Obesity; Nesfatin-1; Peroxisome proliferator-activated receptor γ; Lipid metabolism; Blood lipids
分类号:
R -33
DOI:
DOI:10.3969/j.issn.1000-7377.2025.06.005
文献标志码:
A
摘要:
目的：探讨摄食抑制因子1（Nesfatin-1）对肥胖症大鼠脂代谢的影响，并基于过氧化物酶体增殖物激活受体γ（PPARγ）信号通路探讨其潜在机制。方法：采用高脂饮食建立肥胖症大鼠模型。将造模成功的SD雄性大鼠随机分为模型组、Nesfatin-1低剂量组、Nesfatin-1中剂量组和Nesfatin-1高剂量组，每组10只。另选10只正常大鼠为对照组。Nesfatin-1低、中、高剂量组大鼠尾静脉注射Nesfatin-1（1、10、100 μg/kg），对照组和模型组大鼠注射等量0.9%氯化钠溶液，每天1次，连续21 d。给药期间，记录各组大鼠的体重和摄食量。给药结束后，计算各组大鼠肝脏系数；HE染色观察各组大鼠肝和脂肪组织的病理变化；酶联免疫吸附法（ELISA）检测各组大鼠血脂水平[总胆固醇（TC）、甘油三酯（TG）]、血清游离脂肪酸（FFA）水平及空腹血糖（FBG）、空腹胰岛素（FINS）水平；Western blot检测PPARγ及其靶标脂肪甘油三酯脂肪酶（ATGL）、脂蛋白脂肪酶（LPL）蛋白相对表达量。结果：与对照组比较，模型组大鼠体重、摄食量、肝脏系数、血脂水平、FFA、FBG、FINS水平显著升高（均P<0.05），肝和脂肪组织细胞空泡面积明显增加，PPARγ及其靶标ATGL、LPL蛋白相对表达量显著降低（均P<0.05）。与模型组比较，Nesfatin-1低、中、高剂量组大鼠的体重、摄食量显著降低（均P<0.05），肝和脂肪组织细胞空泡面积明显减少，Nesfatin-1中、高剂量组大鼠的肝脏系数、血脂水平、FFA、FBG、FINS水平显著降低（均P<0.05），PPARγ及其靶标ATGL、LPL蛋白相对表达量显著升高（均P<0.05）。Nesfatin-1高剂量组对大鼠肥胖症的改善效果优于低、中剂量组。结论：Nesfatin-1干预可抑制肥胖症大鼠的体重增长，减少摄食量，降低血脂水平，其机制可能与激活PPARγ信号通路有关。
Abstract:
Objective:To investigate the effect of Nesfatin-1 on lipid metabolism in obese rats and the underlying mechanism based on peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway.Methods：Rat model of obesity was induced by high-fat diet.Successfully modeled SD male rats were randomly divided into model group,low-dose Nesfatin-1 group,medium-dose Nesfatin-1 group,and high-dose Nesfatin-1 group,with 10 rats in each group.Additionally,10 normal rats were selected as the control group.Rats in the low-,medium-,and high-dose Nesfatin-1 groups received tail vein injections of Nesfatin-1 (1,10,100 μg/kg),while rats in the control and model groups received equal volume of 0.9% sodium chloride solution,once daily for 21 consecutive days.During the administration period,the body weight and food intake of rats in each group were recorded.After the administration,the liver coefficient of rats in each group was calculated;pathological changes in the liver and adipose tissue of rats in each group were observed via HE staining;ELISA was used to measure the blood lipid levels (including TC and TG),FFA level,as well as FBG and FINS levels in rats from each group;Western blot was used to detect the relative protein expression levesl of PPARγ and its target genes adipose triglyceride lipase (ATGL) and lipoprotein lipase (LPL).Results:Compared with the control group,the model group exhibited significantly increased body weight,food intake,liver coefficient,blood lipid levels,FFA,FBG,and FINS levels in rats (all P<0.05),and there was notable increase in the vacuolar area of hepatocytes and adipocytes,accompanied by significant decrease in the relative expression of PPARγ and its target proteins ATGL and LPL (all P<0.05).Compared with the model group,the body weight and food intake of rats in the low-,medium-,and high-dose Nesfatin-1 groups were significantly reduced (all P<0.05),and the vacuolar area of liver and adipose tissue cells was markedly decreased;in the medium- and high-dose Nesfatin-1 groups,the liver coefficient,blood lipid levels,FFA level,FBGand FINS levels were significantly decreased (all P<0.05),while the relative protein expression levels of PPARγ and its target genes ATGL and LPL were significantly increased (all P<0.05).The improvement effect of in high-dose Nesfatin-1 group on obesity was better than that in low- and medium-dose groups.Conclusion:Nesfatin-1 can inhibit the body weight gain,reduce food intake and blood lipid levels in obese rats,and the mechanism may be related to the activation of PPARγ signaling pathway.

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备注/Memo

备注/Memo:
云南省卫生健康委员会临床医学中心建设项目（202101AF291051）
更新日期/Last Update: 2025-06-04