Dr. Zeljko Reiner,
This session presented the current situation in serum lipoprotein research and the importance of dyslipidemia for CVD based upon recent findings.
R. Frikke-Schmidt from Copenhagen, Denmark presented an overview of genes affecting levels of LDL cholesterol (well established genes such as those for LDLR and Apo B and new ones, such as as those for PCSK9, LDLRAP1 and ABCG5/8), genes affecting triglycerides (well established genes such as those for LPL,Apo C II and Apo E and new ones such as those for Apo A V, USF1 and ANGPTL4), and genes affecting levels of HDL cholesterol (well established genes such as those for Apo A I, LCAT and ABCA1 and just indicated the possibility of some “new” genes).
J. Boren from Goteborg, Sweden stressed the well known fact that dyslipidemia in type 2 diabetes and insulin resistance is characterized by an increase in triglycerides, low HDL cholesterol, and increased atherogenic small dense LDL particles. He presented new results explaining the mechanisms of overproduction of VLDL1 – a high content of liver fat causes the suppression of conversion of VLDL2 into VLDL1 caused by insulin in healthy liver to be ineffective and an elevation of VLDL1 occurs. This causes an increase in plasma triglycerides, production of slowly metabolised LDL particles which results in producing small, dense LDL particles and an enhanced catabolism of HDL resulting in increase of HDL cholesterol.
U. Beisiegel from Hamburg, Germany presented the results on prolonged postprandial lipemia as an independent risk factor for CVD. Since postprandial hyperlidemia is a characteristic of diabetes and postprandial hypertriglyceridemia is dependent upon the quality of dietary lipids, these results are relevant especially for diabetics.
L. Tokgozoglu from Ankara, Turkey gave an overview of the latest studies on lipoproteins as a risk factor for CVD. She stressed especially the role of low HDL and the current possibilities to raise it, but warned that HDL might be proinflammatory. She also discussed triglycerides as a risk factor pointing out that they are not only linked to HDL and insulin resistance, but that increased nonfasting triglycerides are associated with increased remnants and thus with CVD risk.
Despite the necessity to always determine the global risk, dyslipidemia has to be considered as the most important single risk factor for CVD. Although a lot of research has been done and many aspects of dyslipidemia have been elucidated, there are still some open questions about how some of the lipoproteins participate in atherogenesis.
Lipids. Still relevant in 2007? Symposium - Bench to Bedside
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