The realities of dyslipidaemia in metabolic syndrome and diabetes

Abstract

High-density lipoprotein (HDL) removes excess cholesterol from macrophages in the artery wall, thereby reducing the rate of development of the cholesterol from macrophages in the artery wall, thereby reducing the rate of development of the atherosclerotic plaque. Other anti-atherogenic actions of HDL include preservation of endothelial function, inhibition of the recruitment of inflammatory cells to the developing plaque, antioxidant effects, and antithrombotic effects. Not surprisingly, large epidemiological cohort studies have identified low HDL-cholesterol (HDL-C) as a risk factor for coronary heart disease independently of levels of low-density lipoprotein cholesterol (LDL-C). Low HDL-C frequently occurs together with elevated triglycerides and the appearance of small, dense LDL, as a direct result of the metabolic changes associated with insulin resistance in conditions such as type 2 diabetes and the metabolic syndrome. The worldwide increase in these conditions and the associated increase in prevalence of low HDL-C have resulted in HDL being considered as a target for therapeutic intervention. Correction of low HDL-C should be an important target for therapy, especially in patients with type 2 diabetes and the metabolic syndrome.