Mannose binding lectin deficiency and triglyceride-rich lipoprotein metabolism in normolipidemic subjects

Mannose binding lectin (MBL) is one of the three initiators of complement activation and is therefore closely linked to inflammation. MBL deficiency has been associated with the generation of atherosclerosis. Since atherosclerosis, the complement system and postprandial lipemia are linked to inflammation, we studied postprandial lipoprotein metabolism in MBL deficiency. An observational study was carried out in 107 volunteers (21% MBL deficient). Classical cardiovascular risk factors were not different between subjects with and without MBL deficiency. Oral fat loading tests in 8 MBL deficient and 14 MBL sufficient subjects showed similar postprandial triglyceride, free fatty acid, hydroxybutyric acid and complement component 3 concentrations. MBL deficient subjects had 2.4 times lower postprandial Sf > 400 (chylomicron)–apoB48 concentrations, but in contrast a 2–3.5 times increased Sf 60–400 (VLDL1–TG) and Sf 60–400–apoB100 response. MBL activity was inversely related to the postprandial Sf 60–400–TG increase. Despite lower postprandial Sf > 400–apoB48 concentrations, MBL deficient subjects show an accumulation of Sf 60–400 lipoproteins.