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提取物通过靶向高脂饮食喂养小鼠的脂肪生成途径和肠道菌群失调来减轻肥胖。

Extract Attenuates Obesity by Targeting Adipogenic Pathways and Gut Dysbiosis in High-Fat Diet-Fed Mice.

作者信息

Lin Kuen-Tze, Lee Shih-Yu, Ya-Jy Lee, Wu Po-Jui, Chang Tsu-Chung, Chang Wen-Liang, Yen I-Chuan

机构信息

Department of Radiation Oncology, Cardinal Tien Hospital, New Taipei City 23148, Taiwan.

School of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei City 24205, Taiwan.

出版信息

Int J Mol Sci. 2025 Jun 18;26(12):5856. doi: 10.3390/ijms26125856.

DOI:10.3390/ijms26125856
PMID:40565319
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12193264/
Abstract

Obesity is a major metabolic disorder driven by excessive adipogenesis and lipid accumulation. This study investigated the anti-obesity effects and molecular mechanisms of alcohol extract (ACE) in 3T3-L1 preadipocytes and a high-fat diet (HFD)-induced obesity mouse model. In vitro, alcohol extract significantly inhibited adipocyte differentiation and lipid accumulation in 3T3-L1 cells by downregulating PPARγ and C/EBPα, while activating the AMPK pathway and suppressing MAPK signaling. In vivo, alcohol extract administration reduced body weight, adipose tissue mass, and liver lipid accumulation in high-fat diet-fed mice, ameliorating non-alcoholic fatty liver disease (NAFLD) symptoms. Transcriptomic analysis of adipose tissue revealed that alcohol extract modulated key gene expression profiles related to fatty acid metabolism and adipogenesis, suppressing lipid synthesis while enhancing β-oxidation. Furthermore, alcohol extract rebalanced gut microbiota, increasing beneficial bacterial populations such as and , while reducing pro-inflammatory species. These findings demonstrate that alcohol extract exerts multifaceted anti-obesity effects by regulating lipid metabolism, adipogenesis pathways, and gut microbiota composition, highlighting its potential as a natural therapeutic agent for obesity management.

摘要

肥胖是一种由过度脂肪生成和脂质堆积驱动的主要代谢紊乱疾病。本研究调查了酒精提取物(ACE)在3T3-L1前脂肪细胞和高脂饮食(HFD)诱导的肥胖小鼠模型中的抗肥胖作用及分子机制。在体外,酒精提取物通过下调PPARγ和C/EBPα,同时激活AMPK途径并抑制MAPK信号传导,显著抑制3T3-L1细胞中的脂肪细胞分化和脂质堆积。在体内,给予酒精提取物可降低高脂饮食喂养小鼠的体重、脂肪组织质量和肝脏脂质堆积,改善非酒精性脂肪性肝病(NAFLD)症状。脂肪组织的转录组分析表明,酒精提取物调节了与脂肪酸代谢和脂肪生成相关的关键基因表达谱,抑制脂质合成同时增强β-氧化。此外,酒精提取物使肠道微生物群重新平衡,增加了有益细菌种群,如 和 ,同时减少了促炎 物种。这些发现表明,酒精提取物通过调节脂质代谢、脂肪生成途径和肠道微生物群组成发挥多方面的抗肥胖作用,突出了其作为肥胖管理天然治疗剂的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/406a4aa5fb93/ijms-26-05856-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/86e2b54f5fa1/ijms-26-05856-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/c281b2c38829/ijms-26-05856-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/8b3ecb6c3b4d/ijms-26-05856-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/ec753683728b/ijms-26-05856-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/b2167db7188f/ijms-26-05856-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/c9bb0d3f3bfa/ijms-26-05856-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/67c7751b5762/ijms-26-05856-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/406a4aa5fb93/ijms-26-05856-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/86e2b54f5fa1/ijms-26-05856-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/c281b2c38829/ijms-26-05856-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/8b3ecb6c3b4d/ijms-26-05856-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/ec753683728b/ijms-26-05856-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/b2167db7188f/ijms-26-05856-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/c9bb0d3f3bfa/ijms-26-05856-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/67c7751b5762/ijms-26-05856-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d8/12193264/406a4aa5fb93/ijms-26-05856-g008.jpg

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