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Published on: February 3, 2017
Cardiac IGF-I manipulation by growth hormone following myocardial infarction
K G Matthews1, G P Devlin, S P Stuart
1Functional Muscle Genomics Group, AgResearch Ruakura, Private Bag 3123, East Street, Hamilton, New Zealand.
Insights
Growth hormone (GH) treatment post-myocardial infarction increased IGF-I levels and caused significant cardiomyocyte hypertrophy in sheep. This cardiac growth correlated with local IGF-I expression.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Growth hormone (GH) influences cardiac structure and function, with excess or deficiency linked to reduced lifespan.
- The specific role of GH in the context of myocardial infarction (heart attack) remains unclear.
Purpose of the Study:
- To investigate the effects of GH treatment on the ischaemic heart in a sheep model of myocardial infarction.
Main Methods:
- Sheep with induced myocardial infarction received 30 days of GH treatment.
- Measurements included circulating IGF-I levels, heart weight, cardiomyocyte size, and IGF-I mRNA expression in cardiac tissue.
Main Results:
- GH treatment significantly elevated circulating IGF-I levels (P<0.01) and heart weight (P<0.01).
- A significant increase in cardiomyocyte cross-sectional area (P<0.001) and peri-infarct IGF-I mRNA (P<0.05) was observed.
- Cardiomyocyte hypertrophy was evident post-treatment.
Conclusions:
- Post-infarct GH administration boosts circulating and cardiac IGF-I levels, promoting cardiomyocyte hypertrophy.
- The observed increase in cardiomyocyte size correlates more closely with local cardiac IGF-I expression than with plasma IGF-I levels.
Abstract:
Evidence of a role for growth hormone (GH) in cardiac structure and function has been derived from studies of patients suffering either GH excess or deficiency, both of which may lead to reduced life expectancy. The role of GH in the ischaemic heart, however, is less than clear. We therefore investigated the effect of 30 days GH treatment in sheep with myocardial infarction. GH treatment significantly increased circulating IGF-I levels (P<0.01), heart weight (P<0.01), and cardiomyocyte cross-sectional area (P<0.001). IGF-I mRNA in peri-infarct cardiac tissue also increased significantly (P<0.05). We conclude that post-infarct GH treatment increases circulating and cardiac IGF-I levels, resulting in significant cardiomyocyte hypertrophy. This increase in cardiomyocyte size appears to correlate with local IGF-I expression rather than plasma IGF-I levels.
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