Type 2 diabetes is characterized by impaired endothelial dependent vasodila
tation which may contribute to the high prevalence of vascular disease in s
uch patients. Although hyperglycaemia, dyslipidaemia and hypertension can a
ll independently cause a similar defect, recent data suggest that endotheli
al dysfunction may be intrinsic to the insulin resistance syndrome that com
monly precedes type 2 diabetes. Such abnormalities in endothelial function
could represent the impact of subclinical disturbance of metabolism or alte
rnatively the presence of a common cellular defect that influences both nit
ric oxide bioavailability and insulin mediated glucose disposal. Resolution
of this puzzle is likely to lead to important advances in our knowledge an
d ultimately treatment of vascular disease.