PubMed · 14938900
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C F WILKINSON. 1952. Arteriosclerosis.. https://pubmed.ncbi.nlm.nih.gov/14938900/
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OBJECTIVE: We tested the hypothesis that transendothelial exchange of low-density lipoprotein (LDL) is influenced by the presence of severe atherosclerosis; we previously found this exchange elevated in diabetes patients. METHODS: By an in vivo isotope method, we compared transendothelial LDL exchange in 24 patients with angiographically verified coronary atherosclerosis, 11 patients with angiographically verified peripheral atherosclerosis, 60 patients with diabetes, and in 42 controls. Autologous 131-iodinated LDL ((131)I-LDL) and 125-iodinated albumin ((125)I-albumin) were injected intravenously (i.v.), and the 1-h fractional escape rates (FER(LDL) and FER(alb)) were taken as indices of transendothelial exchange. RESULTS: Patients with coronary or peripheral atherosclerosis had FER(LDL) similar to that of controls [4.3 (3.5-5.1) and 3.2 (2.3-4.1) versus 4.2 (3.7-4.7)%/h; P>0.05], even after adjustment for LDL distribution volume (DV(LDL)). In contrast, diabetes patients had significantly higher FER(LDL) than controls [5.2 (4.6-5.7) versus 4.2 (3.7-4.7)%/h; P<0.05]. This difference was even more pronounced after correction for the distribution volume of LDL. Compared with controls, FER(alb) was not elevated in patients with coronary atherosclerosis, possibly elevated in patients with peripheral atherosclerosis, but was elevated in diabetes patients. There was a tight positive correlation between FER(LDL) and FER(alb) in all groups of patients and controls. CONCLUSION: Transendothelial exchange of low-density lipoprotein is not elevated in patients having severe atherosclerosis. This suggests that the observed vascular leakiness in diabetes precedes and possibly contributes to accelerated atherosclerosis in diabetes.
The oxidation of low-density lipoprotein (LDL) is centrally involved in the initiation and progression of atherosclerosis. High-density lipoprotein (HDL) paraoxonase 1 (PON1) retards the oxidation of LDL and is a major antiatherosclerotic component of HDL. The PON1 gene contains a number of functional polymorphisms in both the coding and the promoter regions, which affect either the level or the substrate specificity of PON1. Genetic case-control and prospective studies conducted to date have produced confusing results. Meta-analysis of these studies indicates no simple relationship between the PON1 polymorphisms and the presence of coronary heart disease (CHD). However, at the present moment in time, it seems that PON1 status, i.e., activity and/or concentration, is more closely related to CHD, and indeed, PON1 has shown to be an independent risk factor for CHD in a prospective study, compared to the genetic polymorphisms. PON1 levels can also be modulated by environmental\lifestyle and possibly pharmaceutical factors. Larger, better designed, preferably prospective studies are needed to determine further the association of PON1 genetic polymorphisms and status with CHD.