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Cardiac peroxisomal enzymes and starvation
M Crescimanno1, M G Armata, L Rausa
1Istituto di Farmacologia e Sezione Autonoma di Oncologia Clinica, Palermo, Italy.
Free Radical Research Communications
|January 1, 1989
Summary
Fasting increases cardiac fatty acyl CoA-oxidase and catalase in mice, leading to higher hydrogen peroxide production. Refeeding reduces this effect, suggesting a role in starvation-induced heart injury.
Area of Science:
- Biochemistry
- Cardiology
- Cellular Metabolism
Background:
- Food deprivation leads to increased plasma free fatty acids.
- Cardiac metabolism adapts to nutrient availability.
- Peroxisomal beta-oxidation plays a role in fatty acid metabolism.
Purpose of the Study:
- To investigate the impact of food deprivation on cardiac peroxisomal enzyme activity.
- To explore the relationship between free fatty acids and hydrogen peroxide production in the heart during starvation.
- To understand the potential mechanisms of myocardial injury during starvation.
Main Methods:
- Mice were subjected to 3-day food deprivation.
- Plasma free fatty acids were measured.
- Cardiac fatty acyl CoA-oxidase and catalase activities were assessed.
- Hydrogen peroxide production in the heart was stimulated and measured.
- Effects of refeeding were evaluated.
Main Results:
- Food deprivation increased plasma free fatty acids.
- Cardiac fatty acyl CoA-oxidase and catalase activities rose significantly (+15.2% and +136.2%, respectively).
- Hydrogen peroxide production in the heart was stimulated after 30 hours of fasting, and this was reversed by 6 hours of refeeding.
Conclusions:
- High myocardial free fatty acid loads during starvation activate peroxisomal beta-oxidation enzymes.
- Increased hydrogen peroxide production by the heart during fasting may contribute to myocardial injury.
- These findings highlight the metabolic adaptations and potential damage in the heart during starvation.