Aims/hypothesis. We investigated the effect of physiological hyperinsulinaemia on global and regional myocardial blood flow and glucose uptake in five patients with Type II (non-insulin-dependent) diabetes mellitus and seven healthy control subjects.

Methods. Myocardial blood flow was assessed by positron emission tomography with oxygen-15 labelled water (H₂ ¹⁵O) either before or after 1 h of euglycaemic hyperinsulinaemia. Myocardial glucose uptake was assessed by positron emission tomography and fluorine-18 labelled fluorodeoxyglucose (¹⁸FDG).

Results. During hyperinsulinaemia, myocardial blood flow increased from 0.91±0.03 to 1.00±0.03 ml^.min^–1.g^–1 in control subjects (p<0.005) and from 0.81±0.02 to 0.95±0.04 ml^.min^–1.g^–1 in diabetic patients (p<0.0005). Corresponding glucose uptakes were 0.56±0.01 and 0.36±0.02 µmol^.min^–1.g^–1 (p<0.0001), respectively. During hyperinsulinaemia, the regional distribution of myocardial blood flow and glucose uptake showed higher values in the septum and anterolateral wall (short axis) and in the mid-ventricle (long axis) in control subjects, and insulin action was circumscribed to these regions. In diabetic patients, the regional distribution of glucose uptake was similar; however, insulin-induced increase of myocardial blood flow was mainly directed to the postero-inferior areas (short axis) and to the base (long axis) of the heart, thus cancelling the predominance of the anterior wall observed before insulin administration.

Conclusion/interpretation. These results provide evidence that insulin-mediated regulation of global myocardial blood flow is preserved in Type II diabetic patients. In contrast, the regional re-distribution of myocardial blood flow induced by insulin is directed to different target areas when compared with healthy subjects, thereby resulting in a mismatch between blood flow and glucose metabolism.