title: Impact of type 2 diabetes on myocardial insulin sensitivity to glucose uptake and perfusion in patients with coronary artery disease.
abstract: OBJECTIVE
  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).
  
  
  CONCLUSIONS
  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.affiliation: Department of Cardiology B, Aarhus University Hospital (SKS), Brendstrupgaardsvej 100, DK-8200 Aarhus N, Denmark.
authors.forename: Hanne M
authors.initials: HM
authors.lastname: Søndergaard
authors.forename: Morten
authors.initials: M
authors.lastname: Bøttcher
authors.forename: Mette
authors.initials: M
authors.lastname: Marie Madsen
authors.forename: Ole
authors.initials: O
authors.lastname: Schmitz
authors.forename: Søren B
authors.initials: SB
authors.lastname: Hansen
authors.forename: Torsten T
authors.initials: TT
authors.lastname: Nielsen
authors.forename: Hans Erik
authors.initials: HE
authors.lastname: Bøtker
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D003324:Coronary Artery Disease / Q000150:complications* / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000378:metabolism*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics; D005947:Glucose / Q000378:metabolism*; D006339:Heart Rate; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion / Q000379:methods; D049268:Positron-Emission Tomography
chemical_list: D001786:Blood Glucose; D019788:Fluorodeoxyglucose F18; D005947:Glucose