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1 Department of Cardiology, Skejby Hospital, University Hospital in Aarhus, DK-8200 Aarhus N; and 2 Department of Medicine M (Endocrinology and Diabetes) and 3 The PET Centre, Aarhus Kommunehospital, University Hospital in Aarhus, DK-8000 Aarhus C, Denmark
Cardiac muscle is characterized by
insulin resistance in specific heart diseases such as coronary artery
disease and congestive heart failure, but not in generalized disorders
like diabetes mellitus and essential hypertension when cardiac
manifestations are absent. To examine whether the insulin antagonistic
effect of growth hormone (GH) acts upon the heart, we compared
insulin-stimulated whole body and myocardial glucose uptake with and
without GH administration during a 3.5-h euglycemic-hyperinsulinemic
clamp in eight healthy males. Myocardial
2-deoxy-2-[18F]fluoro-D-glucose
uptake was measured with positron emission tomography. The data were
converted to myocardial glucose uptake by tracer kinetic analysis. GH
did not change the rate-pressure product. GH decreased whole body
insulin-stimulated glucose disposal by 26% (48.0 ± 12.1 vs. control
62.8 ± 6.1 µmol · kg
1 · min
1,
P < 0.02). Free fatty acids were suppressed to a similar
extent with and without GH during the insulin clamp. Insulin-stimulated myocardial glucose uptake was similar in the presence and in the absence of GH (0.34 ± 0.05 and 0.31 ± 0.03 µmol · g
1 · min
1,
P = 0.18). In conclusion, GH does not impair insulin-stimulated myocardial glucose uptake despite a considerable whole body insulin antagonistic effect. Myocardial insulin resistance is not an inherent consequence of whole body insulin resistance.
insulin resistance; heart; metabolism; heart failure; positron emission tomography
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