Endothelial inflammation correlates with subject triglycerides and waist size after a high-fat meal

被引:40
|
作者
Wang, Ying I. [1 ]
Schulze, John [1 ]
Raymond, Nadine [1 ]
Tomita, Tyler [1 ]
Tam, Kayan [1 ]
Simon, Scott I. [1 ]
Passerini, Anthony G. [1 ]
机构
[1] Univ Calif Davis, Dept Biomed Engn, Davis, CA 95616 USA
关键词
atherosclerosis; dyslipidemia; triglyceride-rich lipoprotein; vascular cell adhesion molecule-1; tumor necrosis factor-alpha; endothelial cells; CELL-ADHESION MOLECULE-1; NECROSIS-FACTOR-ALPHA; RICH LIPOPROTEINS; HYPERTRIGLYCERIDEMIC SUBJECTS; NONFASTING TRIGLYCERIDES; POSTPRANDIAL STATE; METABOLIC SYNDROME; APOLIPOPROTEIN-E; GENE-EXPRESSION; ATHEROSCLEROSIS;
D O I
10.1152/ajpheart.01036.2010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Wang YI, Schulze J, Raymond N, Tomita T, Tam K, Simon SI, Passerini AG. Endothelial inflammation correlates with subject triglycerides and waist size after a high-fat meal. Am J Physiol Heart Circ Physiol 300: H784-H791, 2011. First published December 17, 2010; doi:10.1152/ajpheart.01036.2010.-A rise in postprandial serum triglycerides (PP-sTG) can potentiate inflammatory responses in vascular endothelial cells (ECs) and thus serves as an independent risk factor for predicting increased cardiovascular morbidity. We examined postprandial triglyceride-rich lipoproteins (PP-TGRLs) in subjects ranging from normal to hypertriglyceridemic for their capacity to alter EC acute inflammatory responses. Cultured human aortic ECs (HAECs) were conditioned with PP-TGRLs isolated from human serum at the peak after a moderately high-fat meal. VLDL particle size increased postprandially and varied directly with the subject's PP-sTG level and waist circumference. PP-TGRL particles bound to HAECs and were internalized via LDL receptor-mediated endocytosis. PP-TGRL alone did not induce an inflammatory response over the range of individuals studied. However, combined with low-dose TNF-alpha stimulation (0.3 ng/ml), it elicited a net 10-15% increase above cytokine alone in the membrane expression of VCAM-1, ICAM-1, and E-selectin, which was not observed with fasting TGRLs. In contrast to upregulation of ICAM-1 and E-selectin, VCAM-1 transcription and expression varied in direct proportion with individual PP-sTG and waist circumference. The extent of monocyte arrest on inflamed HAECs under shear stress also correlated closely with VCAM-1 expression induced by conditioning with PP-TGRL and TNF-alpha stimulation. This ex vivo approach provides a quantitative means to assess an individual's inflammatory potential, revealing a greater propensity for endothelial inflammation in hypertriglyceridemic individuals with abdominal obesity.
引用
收藏
页码:H784 / H791
页数:8
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