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首页> 外文期刊>American Journal of Physiology >Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes.
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Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes.

机译：脂多糖可激活肥胖症和2型糖尿病患者脂肪组织的先天免疫系统反应。

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摘要

Type 2 diabetes (T2DM) is associated with chronic low-grade inflammation. Adipose tissue (AT) may represent an important site of inflammation. 3T3-L1 studies have demonstrated that lipopolysaccharide (LPS) activates toll-like receptors (TLRs) to cause inflammation. For this study, we 1) examined activation of TLRs and adipocytokines by LPS in human abdominal subcutaneous (AbdSc) adipocytes, 2) examined blockade of NF-kappaB in human AbdSc adipocytes, 3) examined the innate immune pathway in AbdSc AT from lean, obese, and T2DM subjects, and 4) examined the association of circulating LPS in T2DM subjects. The findings showed that LPS increased TLR-2 protein expression twofold (P<0.05). Treatment of AbdSc adipocytes with LPS caused a significant increase in TNF-alpha and IL-6 secretion (IL-6, Control: 2.7+/-0.5 vs. LPS: 4.8+/-0.3 ng/ml; P<0.001; TNF-alpha, Control: 1.0+/-0.83 vs. LPS: 32.8+/-6.23 pg/ml; P<0.001). NF-kappaB inhibitor reduced IL-6 in AbdSc adipocytes (Control: 2.7+/-0.5 vs. NF-kappaB inhibitor: 2.1+/-0.4 ng/ml; P<0.001). AbdSc AT protein expression for TLR-2, MyD88, TRAF6, and NF-kappaB was increased in T2DM patients (P<0.05), and TLR-2, TRAF-6, and NF-kappaB were increased in LPS-treated adipocytes (P<0.05). Circulating LPS was 76% higher in T2DM subjects compared with matched controls. LPS correlated with insulin in controls (r=0.678, P<0.0001). Rosiglitazone (RSG) significantly reduced both fasting serum insulin levels (reduced by 51%, P=0.0395) and serum LPS (reduced by 35%, P=0.0139) in a subgroup of previously untreated T2DM patients. In summary, our results suggest that T2DM is associated with increased endotoxemia, with AT able to initiate an innate immune response. Thus, increased adiposity may increase proinflammatory cytokines and therefore contribute to the pathogenic risk of T2DM.
机译：2型糖尿病（T2DM）与慢性轻度炎症相关。脂肪组织（AT）可能代表重要的炎症部位。 3T3-L1研究表明，脂多糖（LPS）激活toll样受体（TLR）引起炎症。在这项研究中，我们1）检查了人腹部皮下（AbdSc）脂肪细胞中LPS对TLRs和脂肪细胞因子的激活，2）检查了人AbdSc脂肪细胞中NF-κB的阻滞，3）检查了来自瘦肉的AbdSc AT中的先天免疫途径，肥胖和T2DM受试者，以及4）检查T2DM受试者中循环LPS的关联。结果表明，LPS使TLR-2蛋白表达增加了两倍（P <0.05）。用LPS处理AbdSc脂肪细胞会导致TNF-α和IL-6分泌显着增加（IL-6，对照：2.7 +/- 0.5 vs. LPS：4.8 +/- 0.3 ng / ml; P <0.001;TNF-α α，对照：1.0 +/- 0.83，相对于LPS：32.8 +/- 6.23 pg / ml; P <0.001）。 NF-kappaB抑制剂可降低AbdSc脂肪细胞中的IL-6（对照组：2.7 +/- 0.5 vs. NF-kappaB抑制剂：2.1 +/- 0.4 ng / ml; P <0.001）。 T2DM患者中TLR-2，MyD88，TRAF6和NF-kappaB的AbdSc AT蛋白表达增加（P <0.05），经LPS处理的脂肪细胞中TLR-2，TRAF-6和NF-kappaB升高（P <0.05）。与匹配的对照组相比，T2DM受试者的循环LPS高出76％。 LPS与对照组的胰岛素相关（r = 0.678，P <0.0001）。罗格列酮（RSG）在先前未治疗的T2DM患者亚组中显着降低了空腹血清胰岛素水平（降低了51％，P = 0.0395）和血清LPS（降低了35％，P = 0.0139）。总之，我们的结果表明T2DM与内毒素血症增加有关，AT能够引发先天性免疫应答。因此，肥胖增加可能会增加促炎细胞因子，从而导致T2DM的致病风险。

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