肥胖者的循环单核细胞处于一种促炎状态
Husam Ghanim1, Ahmad Aljada, Deborah Hofmeyer
1Division of Endocrinology, Diabetes, and Metabolism, State University of New York at Buffalo, NY, USA.
Circulation
|September 15, 2004
概括
肥胖会触发周围血液单核细胞 (MNC) 的炎症状态,其特征是核因子kappaB (NF-kappaB) 活性增加和炎症基因表达升高. 这种炎症与胰岛素抵抗有关,并由自由脂肪酸 (FFAs) 调节.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢性疾病研究研究
- 分子生物学分子生物学
背景情况:
- 肥胖与促进炎症媒介的血水平升高有关,例如瘤缩因子-α (TNF-α),干白素-6 (IL-6) 和C反应蛋白 (CRP).
- 在肥胖个体中研究外周血液单核细胞 (MNC) 的炎症状态对于了解与肥胖有关的并发症至关重要.
研究的目的:
- 为了确定来自肥胖者的外周血液单核细胞 (MNC) 是否表现出一种促炎状态.
- 在肥胖中探索炎症调解剂,体重指数 (BMI),自由脂肪酸 (FFAs) 和胰岛素抵抗 (HOMA-IR) 之间的关系.
主要方法:
- 从肥胖和正常体重的控制对象中分离了外周血液单核细胞 (MNC).
- 评估了核因子kappaB (NF-kappaB) 的结合活性和NF-kappaB-beta (IkappaB-beta) 抑制剂水平.
- 使用RT-PCR和其他测定方法量化了炎症基因 (MIF,IL-6,TNF-alpha,MMP-9) 的mRNA表达和这些媒介的血水平.
- 测量了血葡萄糖,胰岛素,FFAs,以及HOMA-IR.
主要成果:
- 肥胖的受试者在MNC中显示显著增加NF-kappaB结合和减少IkappaB-beta.
- 在肥胖个体的MNC中观察到MIF,IL-6,TNF-alpha和MMP-9的mRNA表达增加.
- 在肥胖组中,MIF,IL-6,TNF-alpha,MMP-9和CRP的血度显著更高.
- 血FFA与BMI,IL-6/TNF-alpha mRNA和血CRP相关,而炎症媒介与BMI和HOMA-IR相关.
结论:
- 肥胖的MNC处于促炎状态,由增加的NF-kappaB激活和炎症基因转录证明.
- 血自由脂肪酸 (FFAs) 在调节肥胖的炎症方面发挥着作用.
- 胰岛素抵抗与肥胖个体的炎症调解剂有显著的关联.
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