Whole body insulin resistance characterizes patients with NIDDM, but it is not known whether insulin also has impaired ability to stimulate myocardial glucose uptake (MGU) in these patients. This study was designed to evaluate MGU as measured by 2-[l8F]flu-oro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET) in patients with NIDDM and stable coronary artery disease (CAD) under standardized metabolic conditions. Eight patients with NIDDM, 11 nondiabetic patients with CAD, and 9 healthy control subjects were enrolled in the study. MGU was quanti-tated in the normal myocardial regions with [18F]FDG and PET and the whole body glucose disposal by glucose-insulin clamp technique (serum insulin, ∼430 pmol/l). Plasma glucose and serum insulin concentrations were comparable in all groups during PET studies. The whole body glucose uptake was 45% lower in NIDDM patients (22 ± 9 pmol · min−1 · kg−1 body wt [mean ± SD]), compared with healthy control subjects (40 ± 17 pmol · min−1 · kg−1 body wt, P < 0.05). In CAD patients, whole body glucose uptake was 30 ± 9 pmol · min−1 · kg−1 body wt (NS between the other groups). MGU was similar in the normal segments in all three groups (69 ± 28 pmol · min−1 · 100 g−1 in NIDDM patients, 72 ± 17 pmol · min−1 · 100 g−1 in CAD patients, and 76 ± 10 pmol. min−1 · 100 g−1 in healthy control subjects, NS). No correlation was found between whole body glucose uptake and MGU. As studied by [18F]FDG PET under stable normoglycemic hyperinsulinemic conditions, MGU is not reduced in patients with NIDDM and CAD in spite of peripheral insulin resistance. These findings suggest that there is no significant defect in MGU in patients with NIDDM.

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