Smoking, inflammatory patterns and postprandial hypertriglyceridemia.
Smoking, inflammatory patterns and postprandial hypertriglyceridemia.
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DOI：
10.1016/j.atherosclerosis.2008.08.005
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发表时间：
2009-04
期刊：
影响因子：
5.3
通讯作者：
Arnett, Donna K.
中科院分区：
文献类型：
--
作者：
Kabagambe, Edmond K.;Ordovas, Jose M.;Tsai, Michael Y.;Borecki, Ingrid B.;Hopkins, Paul N.;Glasser, Stephen P.;Arnett, Donna K.
吸烟与餐后高甘油三酯血症(PPT)增加有关。炎症和胰岛素抵抗是这种现象的潜在“驱动因素”。我们测试了炎症模式和/或胰岛素抵抗是否解释了吸烟对PPT的影响。参加NHLBI降脂药物遗传学和饮食网络(GOLDN)研究的男性和女性(n=1036，年龄49±16岁)。每个参与者都被要求暂停使用降脂药物三周，并得到一杯高脂奶昔(83%脂肪和700千卡/平方米)。测定脂肪负荷后0、3.5、6h的甘油三酯浓度。在基线时测定炎症标志物。用主成分分析从单个炎症标志物(hsCRP、IL-2可溶性受体-α、IL-6、肿瘤坏死因子-α和单核细胞趋化蛋白-1)获得炎症模式。用HOMA方程评估胰岛素抵抗(IR)。重复测量-方差分析用于分析。两种炎症模式，即C反应蛋白-IL-6模式和MCP1-肿瘤坏死因子-α模式。我们发现对甘油三酯有显著的主效应(吸烟和时间)和交互作用(吸烟*时间)(P<；0.01)。从未吸烟者、既往吸烟者和现在吸烟者的多变量调整甘油三酯(mg/dl)浓度在0小时分别为127.38±1.0 4、119.82±1.0 5和134.92±1.0 8；在脂肪负荷后3.5小时分别为229.42±1.0 4、238.39±1.0 5和293.94±1.0 8；在脂肪负荷后6小时分别为194.63±1.0 4、208.38±1.0 5和248.27±1.0 8。在调整了HOMA-IR和/或炎症模式后，吸烟仍然显著，这表明吸烟与PPT独立相关(P<；0.05)。这些数据证实了吸烟者脂肪代谢受损，并表明炎症或胰岛素抵抗以外的机制可能解释了吸烟者中观察到的高甘油三酯血症。
Smoking is associated with increased postprandial hypertriglyceridemia (PPT). Inflammation and insulin resistance are potential “drivers” for this phenomenon. We tested whether inflammatory patterns and/or insulin resistance explain the effect of smoking on PPT. Men and women in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study (n=1036, age 49±16 y) were included. Each participant was asked to suspend use of lipid-lowering drugs for three weeks and was given a high-fat milkshake (83% fat and 700 kcal/m2). Triglyceride concentrations at 0, 3.5 and 6 hr after the fat load were measured. Inflammatory markers were measured at baseline. Principal component analysis was used to derive inflammatory patterns from individual inflammatory markers (hsCRP, IL2 soluble receptor-α, IL6, TNF-α and MCP-1). Insulin resistance (IR) was estimated using the HOMA equation. Repeated measures-ANOVA was used for analyses. Two inflammatory patterns, namely CRP-IL6 pattern and MCP1-TNF-α pattern, were derived. We found significant main (smoking and time) and interaction (smoking*time) effects (P<0.01) for triglycerides. The multivariate-adjusted triglyceride (mg/dl) concentrations (mean ± s.e.m) for never, past and current smokers were 127.38±1.04, 119.82±1.05 and 134.92±1.08 at 0 hr; 229.42±1.04, 238.39±1.05 and 293.94±1.08 at 3.5 hr; and 194.63±1.04, 208.38±1.05 and 248.27±1.08 at 6 hr after the fat load, respectively. Smoking remained significant after adjusting for HOMA-IR and/or inflammatory patterns which showed independent associations with PPT (P<0.05). These data confirm impaired metabolism of fat among smokers and suggest that mechanisms other than inflammation or insulin resistance may explain the observed hypertriglyceridemia among smokers.
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影响因子：
5.3
作者：
Eliasson, B;Mero, N;Smith, U
通讯作者：
Smith, U
影响因子：
5.1
作者：
Lanes, R;Paoli, M;Palacios, A
通讯作者：
Palacios, A
DOI：
10.1016/j.lab.2005.03.009
发表时间：
2005-06-01
期刊：
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
影响因子：
--
作者：
Tsai, MY;Hanson, NQ;Arnett, DK
通讯作者：
Arnett, DK
影响因子：
8.2
作者：
MATTHEWS, DR;HOSKER, JP;TURNER, RC
通讯作者：
TURNER, RC
影响因子：
7.1
作者：
Kabagambe, EK;Baylin, A;Campos, H
通讯作者：
Campos, H