Meet the Mighty Mitochondria: Our Natural Energy Factories

Ever been able to drive your car with no gas? Turn on an unplugged TV? What about grow plants without light? In each case there’s no movement or ability to function without an energy source. The same applies to our bodies! Can you name the fuel we all run on?

The full name is adenosinetriphosphate, or more commonly known as ATP. It’s produced by structures in our cells called mitochondria. All of our organs, bones, tissues and muscles are made of trillions of cells, so we also have trillions of mitochondria working constantly to produce the fuel our cells need to function. (In fact, the brain, heart, muscles and other organs do more extensive work and thus have higher concentrations of mighty mitochondria!)

Mitochondria are amazing multi-taskers. Beyond energy production, they’re also involved in many physiological processes including synthesis of neurotransmitters, lipid (a.k.a. fat) synthesis, calcium regulation, insulin secretion in response to food intake, regulation of cell levels of amino acids and other key substances. (Filler, 2014). Clearly these tiny energy factories play a huge roll in how our bodies function.

You can imagine that any dysfunction to our mitochondria would result in numerous negative consequences beyond having less energy for bodies to work effectively.

Mitochondrial dysfunction is implicated in a host of diseases and conditions, including cancer, diabetes, fibromyalgia, mental disorders (e.g. schizophrenia, bipolar disease, autism) and more. How does this damage happen? Well, it can be due to genetic mutations or environmental and/or pharmacological exposures.

The good news is that our bodies are super machines and mitochondria are typically protected from damage. However, like all machines, external factors can have negative implications. In our next blog post we’ll explore several of the major culprits!

Sources:
Filler, K., Lyon, D., Bennett, J., McCain, N., Elswick, R., Lukkahatai, N., & Saligan, L. N. (2014). Association of mitochondrial dysfunction and fatigue: a review of the literature. BBA clinical, 1, 12-23.