Dietary Inflammatory Index and Biomarkers of Lipoprotein Metabolism, Inflammation and Glucose Homeostasis in Adults.

Dietary Inflammatory Index and Biomarkers of Lipoprotein Metabolism, Inflammation and Glucose Homeostasis in Adults.
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DOI:
10.3390/nu10081033
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发表时间:
2018-08-08
期刊:
影响因子:
5.9
通讯作者:
Perry IJ
Perry IJ
中科院分区:
医学2区
文献类型:
--
作者:
Phillips CM;Shivappa N;Hébert JR;Perry IJ

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越来越多的证据表明饮食和炎症是导致心脏代谢风险的潜在机制。然而,关于饮食炎症潜力,心脏代谢健康和代谢综合征(MetS)风险的生物标志物的报告不一致。我们的目的是在1992名成人的横断面样本中检查食物频率问卷(FFQ)衍生的饮食炎症指数(DII®)、脂蛋白代谢生物标志物、炎症和葡萄糖稳态与MetS风险之间的关系。计算来自FFQ的能量调整DII(E-DII)评分。使用核磁共振(NMR)光谱测量脂蛋白颗粒大小和亚类浓度。测定血清急性期反应物、脂肪细胞因子、促炎细胞因子和白色血细胞(WBC)计数。采用稳态模型评估法(HOMA-IR)计算胰岛素抵抗。我们的数据表明,更多的促炎饮食,反映在更高的E-DII评分,与潜在的促动脉粥样硬化脂蛋白谱相关,其特征是大的极低密度脂蛋白(VLDL),小的致密低密度脂蛋白(LDL)和高密度脂蛋白(HDL)颗粒数量增加,大的LDL和HDL颗粒减少(所有p < 0.001)。炎症分析在E-DII评分较高的患者中发现了一系列不良表型,包括较高的补体成分C3(C3)、C反应蛋白(CRP)(均p < 0.05)、白细胞介素6(IL-6)和肿瘤坏死因子(TNF)-α浓度、较高的WBC计数和中性粒细胞与淋巴细胞比率(NLR)以及较低的脂联素水平(均p < 0.001)。校正潜在混杂因素后,E-DII评分较高的患者MetS风险增加(OR 1.37,95% CI(1.01,1.88),p < 0.05)。总之,习惯性摄入更多的促炎饮食与不利的脂蛋白和炎症特征以及MetS风险增加相关。
Accumulating evidence identifies diet and inflammation as potential mechanisms contributing to cardiometabolic risk. However, inconsistent reports regarding dietary inflammatory potential, biomarkers of cardiometabolic health and metabolic syndrome (MetS) risk exist. Our objective was to examine the relationships between a food frequency questionnaire (FFQ)-derived dietary inflammatory index (DII®), biomarkers of lipoprotein metabolism, inflammation and glucose homeostasis and MetS risk in a cross-sectional sample of 1992 adults. Energy-adjusted DII (E-DII) scores derived from an FFQ were calculated. Lipoprotein particle size and subclass concentrations were measured using nuclear magnetic resonance (NMR) spectroscopy. Serum acute-phase reactants, adipocytokines, pro-inflammatory cytokines and white blood cell (WBC) counts were determined. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Our data indicate that a more pro-inflammatory diet, reflected by higher E-DII scores, was associated with potentially pro-atherogenic lipoprotein profiles characterised by increased numbers of large very low density lipoprotein (VLDL), small dense low density lipoprotein (LDL) and high density lipoprotein (HDL) particles and less large LDL and HDL particles (all p < 0.001). Inflammatory profiling identified a range of adverse phenotypes among those with higher E-DII scores, including higher complement component C3 (C3), C-reactive protein (CRP), (both p < 0.05), interleukin 6 (IL-6) and tumour necrosis factor (TNF)-α concentrations, higher WBC counts and neutrophil to lymphocyte ratio (NLR) and lower adiponectin levels (all p < 0.001). MetS risk was increased among those with higher E-DII scores (OR 1.37, 95% CI (1.01, 1.88), p < 0.05), after adjusting for potential confounders. In conclusion, habitual intake of a more pro-inflammatory diet is associated with unfavourable lipoprotein and inflammatory profiles and increased MetS risk.
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