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Updated: Oct 16, 2026

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
Published on: May 16, 2021
Short-term effects of growth hormone on myocardial glucose uptake in healthy humans
H E Bøtker1, H Wiggers, M Bøttcher
1Department of Cardiology, Skejby Hospital, University Hospital in Aarhus, DK-8200 Aarhus N, Denmark. heb@dadlnet.dk
Insights
Growth hormone (GH) causes whole-body insulin resistance but does not affect insulin-stimulated glucose uptake in the heart. This suggests myocardial insulin resistance is not a direct result of systemic insulin resistance.
Area of Science:
- Cardiology
- Endocrinology
- Metabolism
Background:
- Cardiac muscle exhibits insulin resistance in specific heart conditions like coronary artery disease and congestive heart failure.
- Generalized disorders such as diabetes mellitus and essential hypertension do not inherently cause cardiac insulin resistance without cardiac manifestations.
Purpose of the Study:
- To investigate the insulin-antagonistic effects of growth hormone (GH) on the heart.
- To determine if GH administration impacts insulin-stimulated myocardial glucose uptake.
Main Methods:
- A 3.5-hour euglycemic-hyperinsulinemic clamp was performed on eight healthy males.
- Insulin-stimulated whole-body and myocardial glucose uptake were measured with and without GH administration.
- Myocardial glucose uptake was assessed using positron emission tomography (PET) with 2-deoxy-2-[(18)F]fluoro-D-glucose tracer kinetic analysis.
Main Results:
- GH administration significantly decreased whole-body insulin-stimulated glucose disposal by 26% (P < 0.02).
- GH did not alter the heart's rate-pressure product.
- Insulin-stimulated myocardial glucose uptake remained similar with and without GH administration (P = 0.18).
Conclusions:
- Growth hormone exerts a significant insulin-antagonistic effect on the whole body.
- Despite systemic effects, GH does not impair insulin-stimulated glucose uptake in the heart.
- Myocardial insulin resistance is not an inevitable consequence of whole-body insulin resistance.
Abstract:
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-[(18)F]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 micromol. 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 micromol. 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.
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