In vivo evidence for chylomicrons as mediators of postprandial inflammation

• Postprandial lipemia activates leukocytes, which is linked to atherosclerosis.
• We measured fasting and postprandial lipids and leukocyte activation.
• Fasting triglycerides and apo B48 were related to fasting leukocyte activation.
• In the postprandial state, only apo B48 correlated with leukocyte activation.
• Thus, chylomicron remnants may induce postprandial leukocyte activation.

Background and aimsThe postprandial situation is a pro-inflammatory condition most likely linked to the development of atherosclerosis. We evaluated the relationship between apolipoprotein (apo) B48 and fasting and postprandial leukocyte activation markers.MethodsLeukocyte activation markers and apo B48 were determined in 80 subjects with and without coronary artery disease (CAD). Twelve healthy subjects underwent an oral fat loading test (up to 8 h).ResultsFasting apo B48 was significantly higher in patients with CAD (n = 47, 8.1 ± 5.2 mg/L) than in subjects without CAD (n = 33, 5.9 ± 3.9 mg/L, p = 0.022). Fasting apo B48 and triglycerides correlated positively with fasting monocyte CD11b and neutrophil CD66b expression. Plasma apo B48 and leukocyte activation markers increased after an oral fat load. No correlations were found between fasting or postprandial triglycerides and postprandial leukocyte activation markers. We observed no correlations between postprandial apo B48 and postprandial neutrophil CD11b or CD66b expression.ConclusionThis study suggests that chylomicron remnants may be responsible for postprandial leukocyte activation in the circulation. The postprandial chylomicron response may be a stronger mediator of postprandial inflammation than postprandial triglyceridemia.