Mitochondrial ATP Biosynthesis Is Negatively Associated with FFA in Cardiac and Skeletal Muscle During the Development of Obesity in a Rodent Model
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View abstract on PubMed
Summary
This summary is machine-generated.Sucrose-induced obesity impairs ATP synthesis in skeletal muscle mitochondria due to free fatty acid accumulation and increased IF1 levels, while heart muscle ATP synthesis remains unaffected by diet.
Area Of Science
- Mitochondrial biology
- Metabolic disorders
- Obesity research
Background
- Obesity impacts mitochondrial ATP production via factors like proton leaks from free fatty acids (FFA), uncoupling proteins (UCPs), and ATPase inhibitory factor 1 (IF1).
- Sucrose diet-induced obesity models provide insights into metabolic dysfunction.
Purpose Of The Study
- To investigate the impact of sucrose diet-induced obesity on ATP synthesis rates in skeletal and cardiac muscle mitochondria.
- To determine the time course of mitochondrial dysfunction in response to sucrose feeding.
Main Methods
- Isolation of mitochondria from skeletal and cardiac muscle of rats fed a sucrose diet for varying periods.
- Measurement of ATP synthesis rates and assessment of FFA levels, UCP activity (using GDP), and IF1 content.
Main Results
- A significant decline in skeletal muscle mitochondrial ATP synthesis was observed after 24 weeks of sucrose consumption, correlated with increased FFA.
- Heart muscle mitochondrial ATP synthesis rates decreased with age but were not affected by the sucrose diet.
- Sucrose feeding increased IF1 content in both skeletal and cardiac muscle.
Conclusions
- Accumulation of FFAs in skeletal muscle acts as uncouplers, reducing ATP synthesis rates.
- Increased IF1 in skeletal muscle is a protective response to prevent ATP hydrolysis and conserve energy.
- Cardiac mitochondrial function is resilient to sucrose diet-induced obesity in this model, with age being the primary factor affecting ATP synthesis.
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