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人类脂肪细胞肥大过程中脂肪因子分泌和炎症反应的紊乱。

Disrupted adipokine secretion and inflammatory responses in human adipocyte hypertrophy.

作者信息

Gao Dan, Bing Chen, Griffiths Helen R

机构信息

Institute of Molecular and Translational Medicine, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.

Ministry of Education, Key Laboratory of Environment and Genes Related to Diseases Xi'an Jiaotong University, Xi'an, China.

出版信息

Adipocyte. 2025 Dec;14(1):2485927. doi: 10.1080/21623945.2025.2485927. Epub 2025 Apr 3.

DOI:10.1080/21623945.2025.2485927
PMID:40176539
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11980453/
Abstract

Adipocyte hypertrophy is a critical contributor to obesity-induced inflammation and insulin resistance. This study employed a human adipocyte hypertrophy model to investigate the adipokine release, inflammatory responses, and the intracellular singling pathways. Hypertrophic adipocytes exhibited increased lipid content and lipolysis, a decline of anti-inflammatory adipokine adiponectin release and an increase of pro-inflammatory adipokine leptin release compared to mature adipocytes. Moreover, TNFα and LPS exacerbated the decrease in adiponectin secretion by hypertrophic adipocytes while promoting the secretion of leptin, MCP-1 and IL-6, which is associated with impaired activation of p38 and JNK MAPK and persistent activation of ERK and IκBα in hypertrophic adipocytes. These altered adipokine secretions and inflammatory responses within hypertrophic adipocytes may contribute to adipocyte dysfunction in human obesity.

摘要

脂肪细胞肥大是肥胖诱导的炎症和胰岛素抵抗的关键促成因素。本研究采用人脂肪细胞肥大模型来研究脂肪因子释放、炎症反应及细胞内信号通路。与成熟脂肪细胞相比，肥大的脂肪细胞脂质含量和脂解增加，抗炎脂肪因子脂联素释放减少，促炎脂肪因子瘦素释放增加。此外，肿瘤坏死因子α（TNFα）和脂多糖（LPS）加剧了肥大脂肪细胞脂联素分泌的减少，同时促进了瘦素、单核细胞趋化蛋白-1（MCP-1）和白细胞介素-6（IL-6）的分泌，这与肥大脂肪细胞中p38和c-Jun氨基末端激酶（JNK）丝裂原活化蛋白激酶（MAPK）的激活受损以及细胞外信号调节激酶（ERK）和核因子κB抑制蛋白α（IκBα）的持续激活有关。肥大脂肪细胞内这些改变的脂肪因子分泌和炎症反应可能导致人类肥胖中的脂肪细胞功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/e506ede6acb0/KADI_A_2485927_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/37599ce67bc9/KADI_A_2485927_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/164d9809baae/KADI_A_2485927_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/c8052bbad2eb/KADI_A_2485927_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/e506ede6acb0/KADI_A_2485927_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/37599ce67bc9/KADI_A_2485927_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/164d9809baae/KADI_A_2485927_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/c8052bbad2eb/KADI_A_2485927_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8562/11980453/e506ede6acb0/KADI_A_2485927_F0004_OC.jpg

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