肥満患者の循環する単核細胞は,炎症を誘発する状態にある
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
まとめ
肥満は,外周血液単核細胞 (MNC) の炎症性状態を誘発し,核因子カッパB (NF-kappaB) の活性が増加し,炎症性遺伝子発現が上昇することが特徴です. この炎症はインスリン抵抗性に関連しており,自由脂肪酸 (FFAs) によって調節されます.
科学分野:
- 免疫学 免疫学とは
- メタボリック疾患の研究
- 分子生物学は分子生物学である.
背景:
- 肥満は,腫瘍死滅因子アルファ (TNF-alpha),インタールイキン-6 (IL-6),およびC反応性タンパク質 (CRP) のようなプロ炎症的媒介体の血濃度の上昇と関連しています.
- 肥満患者の周辺血液単核細胞 (MNC) の炎症状態を調査することは,肥満に関連する合併症を理解するために重要である.
研究 の 目的:
- 肥満患者からの外周血液単核細胞 (MNC) が炎症促進状態を示すかどうかを判断する.
- 肥満における炎症媒介体,体量指数 (BMI),自由脂肪酸 (FFAs),およびインスリン抵抗性 (HOMA-IR) の関係を調査する.
主な方法:
- 周周血液単核細胞 (MNC) は,肥満および正常体重のコントロール被験者から分離されました.
- 核因子kappaB (NF-kappaB) の結合活性とNF-kappaB-β (IkappaB-β) の阻害剤のレベルが評価されました.
- 炎症性遺伝子 (MIF,IL-6,TNF-alpha,MMP-9) のmRNA発現と,これらの媒介体の血レベルは,RT-PCRやその他の測定法を使用して定量化されました.
- 血グルコース,インスリン,FFA,HOMA-IRを測定した.
主要な成果:
- 肥満患者では,NF-kappaB結合が著しく上昇し,MNCでIkappaB-βが減少した.
- MIF,IL-6,TNF-alpha,およびMMP-9のmRNA発現の増加は,肥満患者のMNCで観察されました.
- MIF,IL-6,TNF-α,MMP-9,およびCRPの血濃度は,肥満グループでは著しく高かった.
- プラズマFFAはBMI,IL-6/TNF-α mRNA,およびプラズマCRPと相関しており,炎症媒介体はBMIとHOMA-IRと関連していた.
結論:
- 肥満のMNCは,NF-kappaBの活性化と炎症性遺伝子転写の増加によって証明される炎症性状態にあります.
- プラズマフリー脂肪酸 (FFAs) は,肥満における炎症を調節する役割を果たします.
- インスリン抵抗性は,肥満者の炎症媒介者と有意に関連しています.
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