title: Mismatch between insulin-mediated glucose uptake and blood flow in the heart of patients with Type II diabetes.
abstract: OBJECTIVE
  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 (H(2)(15)O) either before or after 1 h of euglycaemic hyperinsulinaemia. Myocardial glucose uptake was assessed by positron emission tomography and fluorine-18 labelled fluorodeoxyglucose ((18)FDG).
  
  
  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 micro mol(.)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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute of Clinical Physiology, National Research Council (CNR), Area di Ricerca San Cataldo, Via Moruzzi 1, 56100 Pisa, Italy. patricia.iozzo@ifc.cnr.it
authors.forename: P
authors.initials: P
authors.lastname: Iozzo
authors.forename: P
authors.initials: P
authors.lastname: Chareonthaitawee
authors.forename: O
authors.initials: O
authors.lastname: Rimoldi
authors.forename: D J
authors.initials: DJ
authors.lastname: Betteridge
authors.forename: P G
authors.initials: PG
authors.lastname: Camici
authors.forename: E
authors.initials: E
authors.lastname: Ferrannini
mesh_terms: D001783:Blood Flow Velocity / Q000187:drug effects*; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D015309:Glucose Clamp Technique; D006321:Heart / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000503:physiopathology; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D018579:Patient Selection; D012016:Reference Values; D012039:Regional Blood Flow / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin