Using Fat For Fuel: The Science Behind Fatty Acid Metabolism

Thursday, June 29, 2017. Author Geraldine Campbell

Sources of healthy fat

Beta-oxidation may sound like a scary scientific phase that you don’t want to learn more about, but if fat loss is your goal, then this is an important process to understand.

Your body uses fat as an energy source during all intensities and durations of activity; but predominantly during low intensity and endurance exercise. The breakdown of fatty acids through beta-oxidation allows the formation of Acetyl-CoA which is be used within oxidative phosphorylation to produce ATP. The key process of getting fatty acids into an activated and usable form to produce ATP is called beta-oxidation.

 

What happens during beta-oxidation?

The fatty acids consumed through our diets begin the process of becoming an energy source by using ATP to convert fatty acids into acyl adenylate in the outer mitochondria. This compound then forms Fatty Acyl-CoA through the enzyme Acyl-CoA synthetase and free Coenzyme A. Acyl-CoA is the important substrate needed within the inner mitochondria to become Acetyl-CoA.

 

How does our body get the Fatty Acyl-CoA to where it needs to be?

A shuttle bus of course! Well…sort of…a shuttle system on the inner mitochondrial membrane overcomes the inability of fatty acids to diffuse into the inner mitochondria. The scientific name for this shuttle system is the carnitine palmitoyltransferase (CPT) system. CPT1 transfers the acyl group from the coenzyme A to carnitine; followed by the translocase molecule transferring the acyl carnitine into the inner mitochondria. It is then converted back into the fatty acyl-CoA by CPTII. Now that it is in the mitochondria, the fatty acyl-CoA can be broken down to form acetyl CoA – the substrate needed to allow ATP formation through oxidative phosphorylation.

The amount of energy beta-oxidation can produce is substantially more than carbohydrates which is why for prolonged exercise, fats are your go-to energy source.

The PPARA gene is a key regulator of almost all the steps involved in beta-oxidation. Carrying the G allele variant PPARA gene is associated with higher levels of the PPARA protein, which explains the greater ability to use fat for fuel by carriers.

What can limit your use of fat as fuel?

CPT1 is the rate limiting step to the breakdown of fatty acids – so any impairment can lead to elevated fatty acids in the muscles; and poorer metabolic health. One factor that impairs CPT1 is hyperinsulinemia which would be characteristic of type II diabetics due to their insulin resistance.

At FitnessGenes, we give you a prediction of your insulin function based upon your genetic and lifestyle information. If you have poor insulin function, you could be impairing your ability to utilize fats as an energy source and could experience higher levels of fatty acids in your body. Following the nutrition and exercise advice we provide will help you maintain or improve your insulin function and help you be metabolically healthy and achieve your desired body composition.

 

If you enjoyed this blog, you can read my other posts here:

Food Cravings

Your lunch break is not just for eating… upgrade it to a runch!

Resistance Band Training

Get to know your heart 

How Alcohol May Be Limiting Your Progress

Running and Genetics 

Mindfulness

Genetic Dominance of East African and Jamaican Runners 

Sprint and Power Performance

The Nordic Diet

Seaweed

Oxidative Stress

 

References

http://handwrittentutorials.com/pdf/pdf_87.pdf

Schulz, H., 1991. Beta oxidation of fatty acids. Biochimica et Biophysica Acta (BBA)-Lipids and Lipid Metabolism, 1081(2), pp.109-120.

http://rogersal.people.cofc.edu/HortonChap16.pdf

Ravussin, E. and Smith, S.R., 2002. Increased fat intake, impaired fat oxidation, and failure of fat cell proliferation result in ectopic fat storage, insulin resistance, and type 2 diabetes mellitus. Annals of the New York Academy of Sciences, 967(1), pp.363-378.

Ruderman, N. and Prentki, M., 2004. AMP kinase and malonyl-CoA: targets for therapy of the metabolic syndrome. Nature reviews Drug discovery, 3(4), pp.340-351.

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