Why the study?
What is the origin and functional effect of chylomicron-like particles in a diabetic patient with severe hypertriglyceridemia compared to typical chylomicrons?
What is the origin and functional effect of chylomicron-like particles in a diabetic patient with severe hypertriglyceridemia compared to typical chylomicrons?
In severe hypertriglyceridemia, chylomicron-like particles may be of liver origin (Apo B-100) rather than intestinal origin and can increase platelet aggregation, potentially contributing to atherothrombotic risk.
May heighten atherothrombotic risk via hepatic-origin particles that boost platelet activity in diabetic hypertriglyceridemia; hypothesis-generating for mechanisms in larger cohorts.
Plasma lipoproteins in a diabetic patient with severe hypertriglyceridemia and turbid, milky plasma were studied and compared with those found in three primary type V hyperlipoproteinemic and in three normal subjects after a fatty meal. All subjects had normal post-heparin lipolytic activity. Lipoprotein electrophoresis of the patient's plasma revealed no chylomicron band, and upon short-time ultracentrifugation the patient's supernatant showed most lipid staining in the pre-beta-lipoprotein region. This supernatant, which in type V hyperlipoproteinemia as well as in normal subjects after a fatty meal, contains a large proportion of apolipoprotein B-48 (of intestinal origin), was found in our patient to contain mostly apolipoprotein B-100 (of liver origin). Upon incubation of normal washed platelets with chylomicrons derived either from type V hyperlipoproteinemic or from normal subjects after a fatty meal, platelet aggregation was decreased, whereas the chylomicron-like particles from the patient increased platelet activity. It is, thus, suggested that the triglyceride-rich, cholesterol-poor lipoproteins are of liver and not of intestinal origin.
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Aviram et al. (1985) studied this question.
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