Impact of Type 2 Diabetes on Myocardial Insulin Sensitivity to Glucose Uptake and Perfusion in Patients with Coronary Artery Disease

• Published in: The journal of clinical endocrinology and metabolism 2006-12, Vol.91 (12), p.4854-4861
• Main Authors: Søndergaard, Hanne M., Bøttcher, Morten, Marie Madsen, Mette, Schmitz, Ole, Hansen, Søren B., Nielsen, Torsten T., Bøtker, Hans Erik
• Format: Article
• Language: English
• Subjects: Aged; Biological and medical sciences; Blood Glucose - analysis; Blood Pressure; Coronary Artery Disease - complications; Coronary Artery Disease - metabolism; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - metabolism; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Female; Fluorodeoxyglucose F18 - pharmacokinetics; Fundamental and applied biological sciences. Psychology; Glucose - metabolism; Heart Rate; Humans; Insulin Resistance; Male; Medical sciences; Middle Aged; Muscle, Skeletal - metabolism; Myocardium - metabolism; Perfusion - methods; Positron-Emission Tomography; Vertebrates: endocrinology
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.2006-1416

Background and Hypothesis: Myocardial insulin resistance (IR) is a feature of coronary artery disease (CAD) with reduced left ventricular ejection fraction (LVEF). Whether type 2 diabetes mellitus (T2DM) with CAD and preserved LVEF induces myocardial IR and whether insulin in these patients acts as a myocardial vasodilator is debated. Methods: We studied 27 CAD patients (LVEF > 50%): 12 with T2DM (CAD+DM), 15 without T2DM (CAD-NoDM). Regional myocardial and skeletal glucose uptake, myocardial and skeletal muscle perfusion were measured with positron emission tomography. Myocardial muscle perfusion was measured at rest and during hyperemia in nonstenotic and stenotic regions with and without acute hyperinsulinemia. Results: Myocardial glucose uptake was similar in CAD+DM and CAD-NoDM in both nonstenotic and stenotic regions [0.38 ± 0.08 and 0.36 ± 0.11 μmol/g·min; P value nonsignificant (NS)] and (0.35 ± 0.09 and 0.37 ± 0.13 μmol/g·min; P = NS). Skeletal glucose uptake was reduced in CAD+DM (0.05 ± 0.04 vs. 0.10 ± 0.05 μmol/g·min; P = 0.02), and likewise, whole-body glucose uptake was reduced in CAD+DM (4.0 ± 2.8 vs. 7.0 ± 2.4 mg/kg·min; P = 0.01). Insulin did not alter myocardial muscle perfusion at rest or during hyperemia. Insulin increased skeletal muscle perfusion in CAD-NoDM (0.11 ± 0.03 vs. 0.06 ± 0.03 ml/g·min; P = 0.02), but not in CAD+DM (0.08 ± 0.04 and 0.09 ± 0.05 ml/g·min; P = NS). Conclusion: Myocardial IR to glucose uptake is not an inherent feature in T2DM patients with preserved LVEF. Acute physiological insulin exposure exerts no coronary vasodilation in CAD patients irrespective of T2DM.