Abstract
Maintaining total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels within healthy limits decreases the risk of atherosclerotic vascular disease (AVD) and cardiovascular (CV) events. The predictive value of elevated TG levels for coronary artery disease (CAD) seen in univariate analysis tends to disappear on multivariate analyses, especially when correction is made for HDL-C.
The relationship between TG and HDL-C is complex and not fully understood. Hydrolysis of TG by lipoprotein lipase converts HDL subclass 3 to a larger lipoprotein enriched in both phospholipid and TG. This process occurs in postprandial lipaemia (PPL). An additional factor for the complex relationship between TGs and CV risk is that the lipoproteins which transport plasma TG (chylomicrons, very low density lipoproteins and their remnants) are heterogeneous particles. Therefore, they may differ in their level of atherogenicity.
PPL is a physiological process during which plasma lipoproteins and their subclasses undergo variations in concentration and composition following consumption of food, particularly fatty food. “Postprandial hyperlipidaemia” is the quantitative/qualitative alteration of this normal process. These lipoprotein alterations could play a role in the development of CV disease (CVD). However, lipid levels used to evaluate CV risk are usually measured in the fasting state.
This review focuses on TG, PPL, postprandial hyperlipidaemia and non-HDL-C, their relationships and potential predictive role in atherogenesis and CVD.
Keywords: Triglycerides, postprandial hyperlipidaemia, high density lipoprotein, non-high density lipoprotein-cholesterol, low density lipoprotein cholesterol (LDL-C).
Current Pharmaceutical Design
Title:Hypertriglyceridaemia, Postprandial Lipaemia and Non-HDL Cholesterol
Volume: 20 Issue: 40
Author(s): Claudia Stefanutti, Giancarlo Labbadia and Vasilios G. Athyros
Affiliation:
Keywords: Triglycerides, postprandial hyperlipidaemia, high density lipoprotein, non-high density lipoprotein-cholesterol, low density lipoprotein cholesterol (LDL-C).
Abstract: Maintaining total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels within healthy limits decreases the risk of atherosclerotic vascular disease (AVD) and cardiovascular (CV) events. The predictive value of elevated TG levels for coronary artery disease (CAD) seen in univariate analysis tends to disappear on multivariate analyses, especially when correction is made for HDL-C.
The relationship between TG and HDL-C is complex and not fully understood. Hydrolysis of TG by lipoprotein lipase converts HDL subclass 3 to a larger lipoprotein enriched in both phospholipid and TG. This process occurs in postprandial lipaemia (PPL). An additional factor for the complex relationship between TGs and CV risk is that the lipoproteins which transport plasma TG (chylomicrons, very low density lipoproteins and their remnants) are heterogeneous particles. Therefore, they may differ in their level of atherogenicity.
PPL is a physiological process during which plasma lipoproteins and their subclasses undergo variations in concentration and composition following consumption of food, particularly fatty food. “Postprandial hyperlipidaemia” is the quantitative/qualitative alteration of this normal process. These lipoprotein alterations could play a role in the development of CV disease (CVD). However, lipid levels used to evaluate CV risk are usually measured in the fasting state.
This review focuses on TG, PPL, postprandial hyperlipidaemia and non-HDL-C, their relationships and potential predictive role in atherogenesis and CVD.
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Cite this article as:
Stefanutti Claudia, Labbadia Giancarlo and Athyros G. Vasilios, Hypertriglyceridaemia, Postprandial Lipaemia and Non-HDL Cholesterol, Current Pharmaceutical Design 2014; 20 (40) . https://dx.doi.org/10.2174/1381612820666140620120130
DOI https://dx.doi.org/10.2174/1381612820666140620120130 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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