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 micromol/g.min; P value nonsignificant (NS)] and (0.35 +/- 0.09 and 0.37 +/- 0.13 micromol/g.min; P = NS). Skeletal glucose uptake was reduced in CAD+DM (0.05 +/- 0.04 vs. 0.10 +/- 0.05 micromol/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.
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 micromol/g.min; P value nonsignificant (NS)] and (0.35 +/- 0.09 and 0.37 +/- 0.13 micromol/g.min; P = NS). Skeletal glucose uptake was reduced in CAD+DM (0.05 +/- 0.04 vs. 0.10 +/- 0.05 micromol/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.
Authors: Roni Nielsen; Anders Jorsal; Peter Iversen; Lars Tolbod; Kirsten Bouchelouche; Jens Sørensen; Hendrik Johannes Harms; Allan Flyvbjerg; Hans Erik Bøtker; Henrik Wiggers Journal: J Nucl Cardiol Date: 2016-07-29 Impact factor: 5.952
Authors: Jan Hansen; Birgitte Brock; Hans Erik Bøtker; Albert Gjedde; Jørgen Rungby; Michael Gejl Journal: Rev Endocr Metab Disord Date: 2014-09 Impact factor: 6.514
Authors: Roni Nielsen; Helene Nørrelund; Ulla Kampmann; Hans Erik Bøtker; Niels Møller; Henrik Wiggers Journal: PLoS One Date: 2013-01-08 Impact factor: 3.240