Calcium in mitochondria governs fat use as energy source, study finds

An international study by the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) and the University of California, Los Angeles (UCLA) has identified a calcium-driven mechanism that regulates how mitochondria interact with lipid droplets to control fat burning. Published in The EMBO Journal, the research reveals that calcium inside mitochondria acts as a molecular switch, determining whether these organelles remain attached to lipid droplets or separate to initiate fat breakdown Source: El Confidencial.

The mechanism

When calcium levels rise inside mitochondria, they change shape and detach from lipid droplets. This separation is essential for lipases to access stored fats and convert them into energy, explained first author Rebeca Acín-Pérez Source: Infobae. The mitochondrial calcium exchanger NCLX controls this process: reduced NCLX activity leads to calcium accumulation, detachment, and increased fat combustion. Conversely, active NCLX promotes attachment. The protein PDE2A indirectly modulates calcium levels Source: El Confidencial.

Implications for obesity

In obese animal models, pharmacological inhibition of PDE2A increased mitochondria-lipid association, reduced fat degradation, and shifted metabolism toward glucose use, improving metabolic control and energy expenditure Source: Infobae. This demonstrates that manipulating the mechanism can have therapeutic potential.

The findings highlight that mitochondria-lipid droplet interaction is dynamic and finely tuned by calcium signals, opening new avenues for obesity treatments.