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High-density lipoproteins (HDL) are believed to protect against atherosclerosis by promoting the process of reverse cholesterol transport. This process involves different steps including efflux of cellular cholesterol, cholesterol esterification and lipid transport and exchange. Apolipoprotein (apo) A-I, the major HDL apolipoprotein, and the HDL-associated enzyme lecithin-cholesterol acyltransferase (LCAT), which uses apo A-I as a cofactor, play a crucial role in reverse cholesterol transport. HDL may be classified into species according to their apolipoprotein content. Recent data concerning HDL particles indicate that lipoproteins containing apo A-I but not apo A-II (LpA-I) are more effective carriers of free cholesterol and are associated with a protective effect against coronary heart disease. In vitro studies have shown that glycosylated HDL are functionally abnormal and may be considered atherogenic. Our study considers the different impacts of non-enzymatic glycosylation of apo A-I or protein-HDL on the reverse cholesterol transport process.

The excess risk of cardiovascular disease in Type 1 diabetes mellitus compared to non diabetic subjects is only partially explained by standard risk factors. Several studies suggest that Lp(a) concentrations are increased in Type 1 diabetes mellitus, but data are still controversial. Moreover, a high cardiovascular risk has been reported in diabetic patients with persistent proteinuria. Therefore, the aim of this study was to compare the Lp(a) particle levels in insulin-dependent diabetic patients with or without increased urinary albumin excretion. Cross-sectional study of Lp(a) plasma levels in a population of 140 insulin-dependent diabetic patients: 83 without increased proteinuria, 14 with borderline elevation of urinary albumin excretion, 27 with micro- and 16 with macro-proteinuria. Simultaneous determination of plasma lipids, fasting blood glucose and HbA1c was performed. The mean plasma Lp(a) concentrations and the distribution of the levels were comparable in all of the diabetic patient groups. No relationship existed between Lp(a) and HbA1c, fasting blood glucose or any lipid plasma levels. No influence of albumin excretion rate on Lp(a) levels was observed. These data provide no evidence of a specific contribution of Lp(a) particles to the increased morbidity and mortality from cardiovascular disease observed among patients with nephropathy.