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Cardiolipin content controls mitochondrial coupling and energetic efficiency in muscle
Alexandre Prola1,2,3, Jordan Blondelle1,2,3, Aymeline Vandestienne1,2,3
1Université Paris-Est Créteil, INSERM, IMRB, Team Relaix, F-94010 Créteil, France.
Science Advances
|February 1, 2021
Summary
Mice lacking a muscle enzyme for very-long-chain fatty acid synthesis showed higher energy expenditure and protection against obesity. This suggests targeting lipid oxidation in muscle could be an obesity treatment strategy.
Area of Science:
- Biochemistry
- Metabolism
- Mitochondrial Biology
Background:
- Obesity is a significant public health issue driven by imbalanced energy partitioning.
- Strategies to increase basal energy expenditure for obesity management face efficiency and safety challenges.
Purpose of the Study:
- To investigate the role of very-long-chain fatty acid synthesis in muscle on energy expenditure and obesity.
- To explore the underlying mechanisms linking muscle very-long-chain fatty acid metabolism to mitochondrial function and obesity.
Main Methods:
- Generated mice deficient in a muscle-specific very-long-chain fatty acid synthesis enzyme.
- Assessed basal energy expenditure and protection against high-fat diet-induced obesity.
- Analyzed mitochondrial cardiolipin content and respiratory chain-ATP synthase coupling efficiency.
Main Results:
- Mice lacking the muscle enzyme exhibited increased basal energy expenditure and resistance to diet-induced obesity.
- This metabolic phenotype was associated with reduced cardiolipin levels in skeletal muscle mitochondria.
- Impaired mitochondrial coupling efficiency was observed, which could be reversed by cardiolipin enrichment.
Conclusions:
- Muscle-specific very-long-chain fatty acid synthesis impacts whole-body energy balance and obesity.
- Modulating cardiolipin-dependent mitochondrial ATP production in skeletal muscle offers a potential therapeutic avenue for obesity.
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