Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance.
Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance.
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DOI：
10.2337/dc09-0979
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发表时间：
2009-12
期刊：
影响因子：
16.2
通讯作者：
Dandona P
中科院分区：
文献类型：
--
作者：
Ghanim H;Abuaysheh S;Sia CL;Korzeniewski K;Chaudhuri A;Fernandez-Real JM;Dandona P
比较高脂高碳水化合物（HFHC）与高纤维和水果粉对内毒素浓度（脂多糖[LPS]），LPS结合蛋白（LBP）的影响，单核细胞中细胞因子信号3（SOCS-3）的TOLL样受体（TLR）和抑制剂。
健康的受试者的饮食量为910卡路里（n = 10）或美国心脏协会（aha） - 在快速收集到1次过夜后，富含纤维和水果的饭菜（n = 10）。餐后2小时，氧化应激的细胞指数；我们测量了。
HFHC粉的摄入量会诱导血浆LPS浓度的增加，SOCS-3，TLR2和TLR4蛋白的表达，反应性氧的产生和核因子-κB结合活性（所有这些增加）是完全不存在的。富含纤维和水果的AHA餐。
HFHC餐后描述的新颖变化进一步阐明了餐后感染的机制，还提供了第一个证据，解释了SOCS-3介导的胰岛素和瘦素耐药性的发病机理，相反，AHA餐食不诱导这些影响。
To compare the effect of a high-fat, high-carbohydrate meal (HFHC) with that of a high-fiber and fruit meal on the concentrations of endotoxin (lipopolysaccharide [LPS]), LPS-binding protein (LBP), the expression of toll-like receptors (TLRs), and the suppressor of cytokine signaling-3 (SOCS-3) in mononuclear cells. Healthy lean subjects were given 910 calories of either an HFHC meal (n = 10) or an American Heart Association (AHA)-recommended meal rich in fiber and fruit (n = 10) after an overnight fast. Blood was collected before and at 1, 2, and 3 h after the meal. Cellular indexes of oxidative and inflammatory stress; the expression of SOCS-3, TLR2, and TLR4 in mononuclear cells; and plasma concentrations of LPS and LBP were measured. HFHC meal intake induced an increase in plasma LPS concentration and the expression of SOCS-3, TLR2, and TLR4 protein, reactive oxygen species generation, and nuclear factor-κB binding activity (P < 0.05 for all). These increases were totally absent after the AHA meal rich in fiber and fruit. The novel changes described after the HFHC meal elucidate further the mechanisms underlying postprandial inflammation and also provide the first evidence explaining the pathogenesis of insulin and leptin resistance mediated by SOCS-3 after such meals. In contrast, an AHA meal does not induce these effects.