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This Article Full Text Full Text (PDF) All Versions of this Article: 291/2/E282    most recent 00604.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Lautamäki, R. Articles by Nuutila, P. Search for Related Content PubMed PubMed Citation Articles by Lautamäki, R. Articles by Nuutila, P.

Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes

¹Turku PET Centre, ²Department of Radiology, University of Turku, Turku, Finland; ³Institute of Clinical Physiology, National Research Council, Pisa, Italy; ⁴Department of Clinical Chemistry, University of Tampere and Tampere University Hospital, Tampere; ⁵Medicity Research Laboratory and Department of Medical Microbiology, University of Turku and Department of Bacterial and Inflammatory Diseases, National Public Health Institute, Turku; and ⁶Department of Medicine, University of Turku, Turku, Finland

Submitted 2 December 2005 ; accepted in final form 7 February 2006

Nonalcoholic fatty liver (NAFL) is a common comorbidity in patients with type 2 diabetes and links to the risk of coronary syndromes. The aim was to determine the manifestations of metabolic syndrome in different organs in patients with liver steatosis. We studied 55 type 2 diabetic patients with coronary artery disease using positron emission tomography. Myocardial perfusion was measured with [¹⁵O]H₂O and myocardial and skeletal muscle glucose uptake with 2-deoxy-2-[¹⁸F]fluoro-D-glucose during hyperinsulinemic euglycemia. Liver fat content was determined by magnetic resonance proton spectroscopy. Patients were divided on the basis of their median (8%) into two groups with low (4.6 ± 2.0%) and high (17.4 ± 8.0%) liver fat content. The groups were well matched for age, BMI, and fasting plasma glucose. In addition to insulin resistance at the whole body level (P = 0.012) and muscle (P = 0.002), the high liver fat group had lower insulin-stimulated myocardial glucose uptake (P = 0.040) and glucose extraction rate (P = 0.0006) compared with the low liver fat group. In multiple regression analysis, liver fat content was the most significant explanatory variable for myocardial insulin resistance. In addition, the high liver fat group had increased concentrations of high sensitivity C-reactive protein, soluble forms of E-selectin, vascular adhesion protein-1, and intercellular adhesion molecule-1 (P < 0.05) and lower coronary flow reserve (P = 0.02) compared with the low liver fat group. In conclusion, in patients with type 2 diabetes and coronary artery disease, liver fat content is a novel independent indicator of myocardial insulin resistance and reduced coronary functional capacity. Further studies will reveal the effect of hepatic fat reduction on myocardial metabolism and coronary function.

hepatic steatosis; coronary disease; positron emission tomography; magnetic resonance spectroscopy