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1.
Atherosclerosis ; 208(1): 3-9, 2010 Jan.
Article in English | MEDLINE | ID: mdl-19595353

ABSTRACT

Coronary heart disease (CHD) is a leading cause of death in western societies. In the last few decades, a number of epidemiological studies have shown that a disproportion between atheroprotective and atherogenic lipoproteins in plasma is one of the most important contributors towards atherosclerosis and CHD. Thus, based on the classical view, reduced HDL cholesterol levels independently predict one's risk factor for developing cardiovascular disease, while elevated HDL levels protect from atherosclerosis. However, more recent studies have suggested that the relationship between HDL and cardiovascular risk is more complex and extends beyond the levels of HDL in plasma. These studies challenge the existing view on HDL and cardiovascular risk and trigger a discussion as to whether low HDL is a causal effect for the development of heart disease. In this article we provide a review of the current literature on the biogenesis of HDL and its proposed functions in atheroprotection. In addition, we discuss the significance of both HDL quality and quantity in assessing cardiovascular risk.


Subject(s)
Atherosclerosis/metabolism , Lipoproteins, HDL/biosynthesis , Atherosclerosis/complications , Coronary Disease/etiology , Humans , Lipoproteins, HDL/physiology
2.
FEBS J ; 276(20): 5720-8, 2009 Oct.
Article in English | MEDLINE | ID: mdl-19754875

ABSTRACT

Apolipoprotein E is a polymorphic glycoprotein in humans with a molecular mass of 34.5 kDa. It is a component of chylomicron remnants, very low density lipoprotein, low density lipoprotein and high density lipoprotein, and is primarily responsible for maintaining plasma lipid homeostasis. In addition to these well-documented functions, recent studies in experimental mouse models, as well as population studies, show that apolipoprotein E also plays an important role in the development of obesity and insulin resistance. It is widely accepted that disruption in homeostasis between food intake and energy expenditure, and the subsequent deposition of excess fatty acids into fat cells in the form of triglycerides, leads to the development of obesity. Despite the pivotal role of obesity and dyslipidemia in the development of the metabolic syndrome and heart disease, the functional interactions between adipose tissue and components of the lipoprotein transport system have not yet been investigated thoroughly. In this minireview, we focus on the current literature pertinent to the involvement of apolipoprotein E in the development of pathologies associated with the metabolic syndrome.


Subject(s)
Apolipoproteins E/physiology , Obesity/metabolism , Obesity/pathology , Animals , Apolipoproteins E/genetics , Apolipoproteins E/metabolism , Humans , Insulin Resistance/genetics , Insulin Resistance/physiology , Mice , Obesity/etiology
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