Dyslipidaemia in the metabolic syndrome and type 2 diabetes: pathogenesis, priorities, pharmacotherapies.

IMPORTANCE OF THE FIELD

Dyslipoproteinaemia is a cardinal feature of the metabolic syndrome that accelerates atherosclerosis. It is usually characterized by high plasma concentrations of triglyceride-rich and apolipoprotein B (apoB)-containing lipoproteins, with depressed concentrations of high-density lipoprotein (HDL). Drug interventions are essential for normalizing metabolic dyslipidaemia.

AREAS COVERED IN THIS REVIEW

This review discusses the mechanisms and treatment for dyslipidaemia in the metabolic syndrome and type 2 diabetes.

WHAT THE READER WILL GAIN

A comprehensive understanding of the pathophysiology and pharmacotherapy of dyslipidaemia in the metabolic syndrome and diabetes.

TAKE HOME MESSAGE

Dysregulation of lipoprotein metabolism may be due to a combination of overproduction of triglyceride-rich lipoproteins, decreased catabolism of apoB-containing particles, and increased catabolism of HDL particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance and an excess of both visceral and hepatic fat. Lifestyle modifications may favourably alter lipoprotein transport in the metabolic syndrome. Patients with dyslipidaemia and established cardiovascular disease should receive a statin as first-line therapy. Combination with other lipid-regulating agents, such as ezetimibe, fibrates, niacins and fish oils may optimize the benefit of statin on atherogenic dyslipidaemia.