Type II (non-insulin-dependent) diabetes mellitus is associated with a considerably enhanced risk of cardiovascular disease morbidity and mortality. Several epidemiological studies have shown an association between the 2-h glucose value after a 75 gm glucose load (2hPG) and mortality from all causes and from cardiovascular disease. The key question is whether postprandial glucose is related causally to the adverse outcomes (risk factors) or just a marker of risk. Since insulin resistance is one of the determinants of the 2hPG, factors associated with the insulin resistance syndrome, in particular postprandial hypertriglyceridaemia, also need to be considered. Glycaemic excursions could contribute to oxidative stress, endothelial dysfunction, formation of advanced glycation end-products and prolongation of the QTc interval. However, high postprandial concentrations of triglyceride rich lipoproteins, which can be partly attributed to obesity and insulin resistance, have now been recognised to affect endothelial function, to promote atherogenesis, and to be associated with coronary artery disease. On the basis of present evidence Type II diabetic patients require good overall glycaemic control, as reflected by target values of HbA(1 c). However, postprandial hyperglycaemia should be considered as a marker of underlying metabolic abnormalities. Therefore, at present there is no evidence to support the recommendation to consider postprandial hyperglycaemia as a treatment target in itself and would thus require intervention studies showing added benefit of selectively targeting at meal-related glucose excursions in patients with an adequate HbA(1 c). Drugs aiming at improving only postprandial glucose values are not likely to lower the excess mortality associated with Type II diabetes.