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Myocardial Glucose Transport and Utilization in Patients With Type 2 Diabetes Mellitus, Left Ventricular Dysfunction, and Coronary Artery Disease

David P. Dutka, MD, FRCP^_*,_*, Michael Pitt, FRCP, Domenico Pagano, MD, FRCS, Marco Mongillo, MD, PhD, David Gathercole, BSc, PhD, Robert S. Bonser, FRCS, FRCP and Paolo G. Camici, MD, FESC, FACC, FAHA, FRCP

^_* Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, United Kingdom
MRC Clinical Sciences Centre & National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.

View larger version (24K): [in this window] [in a new window] [Download PPT slide]   Figure 1 The distribution of myocardial blood flow (MBF) (A), myocardial glucose utilization (MGU) (B), and glucose extraction (C) during the euglycemic hyperinsulinemic clamp in the patients with and without type 2 diabetes mellitus (T2DM). Ant = anterior regions of the left ventricle; IP = inferoposterior regions of the left ventricle; Lat = lateral regions of the left ventricle.

View larger version (30K): [in this window] [in a new window] [Download PPT slide]   Figure 2 Anti-glucose transporter 4 immunoblot (top) with matching coomassie blue stained gel (bottom) from patients with hibernating myocardium plus in donor myocardium. Immunoblots from diabetic patients are denoted D. Molecular weight standards are shown in the left lane of the gel. Densitometric quantification of the glucose transporter 4 immunoblot was normalized for myosin heavy chain content using the band at 200 kDa on the Coomassie blue stained gel.