Patients with non-insulin dependent (type 2) diabetes have a 2–5-fold increase in age adjusted mortality from coronary heart disease (CHD).1 ,2 CHD accounts for up to 70% of the observed mortality in these patients.1 ,2 The distinct metabolic background of type 2 diabetes appears to be of pathophysiological importance in producing this excess of CHD, and therefore should provide the key to therapeutic intervention for reducing its incidence.

Type 2 diabetes is characterised by, in addition to hyperglycaemia, raised serum triglycerides and reduced high density lipoprotein (HDL) cholesterol compared to people without diabetes.3-5 In contrast, total and low density lipoprotein (LDL) cholesterol concentrations are usually similar to those found in non-diabetic subjects.3-5 The importance of this increase in triglycerides is the metabolic link with the production of remnant particles that are highly atherogenic, a reduced HDL cholesterol, and the production of small dense LDL.5 It is the small dense LDL species (or LDL-III) of LDL particle distribution that is considered to be particularly atherogenic and is more readily oxidised. Additional features of this “diabetic dyslipidaemia”5are increased postprandial lipaemia, compositional changes in very low density lipoprotein (VLDL) and HDL, which are associated with increased coagulant factors—fibrinogen, factor VII, and plasminogen activating factor-I.6

There are considerable epidemiological data linking diabetic dyslipidaemia with the incidence of CHD in type 2 diabetes 2 patients.1 ,2 ,5 In the general population a recent meta-analysis has shown that increased serum triglyceride is an …