Metabolism of Saturated Fat

The Fate of Saturated Fats

What happens to saturated fat when we eat it?

Previously, we looked at the metabolism of glucose. This occurs when you eat carbohydrate as a fuel source.

But as humans, we eat much more than carbohydrates, don’t we? The other types of “macronutrients” that our body uses are fats and proteins. These must go through a metabolism mechanism as well, right?


Saturated Fat Products

The metabolism of protein is not a topic of controversy, so we are going to leave that one alone for right now. Instead, let’s look at something that has caused tons of controversy through recent years: FAT.

Now that we have a basic understanding of your bodily processes, let’s look at what happens to saturated fats.

We go into much greater detail with fat than we did with glucose. Why?

Interestingly enough, every introductory biology book goes into the metabolism of glucose – but it is rare to find one that tells you about the metabolism of fat…

This is an excerpt from Campbell’s Biology in Focus – the introductory bio book we used in school. This was the only thing they had to say about fat metabolism… They don’t go into any more detail.

“A gram of fat oxidized by respiration produces more than twice as much ATP as a gram of carbohydrate.”[1]

You’re kidding me, right?!? That’s all they have to say about using fat for energy?

Angry Child

They have an entire chapter on carbohydrate… and only 3 sentences on fat. Don’t you think they would want to dive into that topic more?

Nope, guess not. They move right on to a new topic after that statement. Conspiracy? Maybe so..

Since they don’t do a good job of teaching you how fat is metabolized in school, we are taking the liberty to teach it to you ourselves.

Below is a summary of how fats go from food to energy.

Eating Saturated Fat

What exactly happens after you eat the fat from your food? Let’s start from the beginning.

The fat you eat comes in the form of a “triglyceride.”

==> That is: a glycerol group attached to 3 fatty acid chains, as shown below:

Saturated fat triglyceride

These beginning processes are the same for all types of fat (regardless of degree of unsaturation).

But for right now, let’s just look at what happens to a saturated fat molecule.

As soon as the fat enters your body, enzymes start to break it down. This process is called “lipolysis.”

It is the breaking down of the fat into its building blocks. The enzyme that does this is called “lipase.”

Useful lipase for these fats are found in your mouth[2], stomach[3][4], and pancreas.[5]

Most of the breaking down of fats occurs in the stomach and small intestine. This is where pancreatic lipase lets loose on the triglyceride.

Once this happens, the glycerol and fatty acid chains are cleaved from one another. They become free fatty acids carried around by albumin (a protein) or chylomicrons in your blood stream.[6]

Albumin is water soluble, and it helps the fatty acids travel around. It takes them either to:

  • the liver for refining and storage
  • elsewhere in your body for energy use

The “elsewhere” in your body is where you generate ATP.

(This is all analogous to how carbohydrate breaks down into glucose… fat breaks down into fatty acids.)

How fat goes into your cell

They float around in the blood until they get to a distant cell in need of energy. 

Getting these fatty acids into the cell involves transport / binding proteins.

These proteins also help with translocation inside the cell.[7][8]

“Fatty acid translocase” helps transport the fatty acid for mitochondrial use.[9]

So far, we have:

Fat  fatty acid (outside cell)  fatty acid (inside cell).

There is a summary diagram to the right. Once the fatty acids are transported from the bloodstream into the cell, the fatty acids start to get processed. Let’s have a look!

Getting the Fatty Acid Ready

Okay, so at this point, our fatty acid is inside of the cell. Awesome!

But it is still outside of the mitochondria, where it needs to end up for energy production. (We are inside the cell, but outside the mitochondria.) Your body needs to prep the fatty acid a bit more before it is used for energy.

Now, it starts to get a bit technical, but we will make sure you can follow along.

The Prep (Before β-Oxidation)[10]:

Diagram of transport of fatty acid into mitochondria

  1. Once the fatty acid is inside the cell, it needs to go through some transformation.
    1. “Coenzyme A (CoA)” attaches to the fatty acid.
      1. “Fatty acyl-CoA synthetase” does the attaching.
      2. The entire complex is called “acyl-CoA.”
    2. Fatty acid → acyl-CoA (outside mitochondria).
  2. The acyl-CoA then has to be altered more (so it can cross through the mitochondrial membrane).
    1. “Carnitine palmitoyltransferase 1” takes that acyl-CoA and converts it into “acyl-carnitine.”
    2. Now it can transport across the mitochondrial membrane.
      1. “Carnitine translocase” has the pleasure of escorting the acyl-carnitine across.
    3. Acyl-CoA (outside mitochondria) → acyl-carnitine (inside mitochondria).
  3. So now that our (modified) fatty acid is inside the mitochondria, it needs to change back to acyl-CoA for β-oxidation.
    1. “Carnitine palmitoyltransferase 2” turns the acyl-carnitine back into acyl-CoA..
    1. Acyl-carnitine → acyl CoA.

We are now ready for beta-oxidation!!!

Dang, that was dense! We do not mean to overwhelm you with the details. Don’t worry too much about them! Believe it or not, this is still just a simplified overview. We don’t go into the specific mechanisms with each step.

The above details are for your reference, but the summaries (bold text) are the main takeaways. It is simple, but sounds complex because of the words. In reality, this is just one big flow process. Use the summary diagram to the right for visual guidance!

[Fun fact: people with a carnitine deficiency are a rare group that cannot be on a ketogenic diet without supplements.]


Okay, so now our fatty acid is inside the mitochondria — all prepped and ready for use. This next chapter of the fatty acid’s life is called “beta-oxidation” (or β-oxidation).

The acyl-CoA (modified fatty acid) will break down into smaller and smaller pieces. The result of this catabolism is the creation of acetyl-CoA.

ATP - the energy of life

Wait a minute. What’s the difference between acyl-CoA and acetyl-CoA? They sound super similar, don’t they?

==> Acyl-CoA is a term for a general long-chain fatty acid with coenzyme A attached at the end.

==> Acetyl-CoA is a very specific molecule: a 2-carbon chain with the coenzyme A attached at the end.

*This acetyl-CoA goes through the Krebs Cycle. Your body generates ATP here. And after the Krebs Cycle, your body generates even more ATP through the electron transport chain.

The metabolism of glucose had the exact same result. (Glucose → acetyl-CoA)

[Check it out here for a quick reminder.]

Remember, ATP is the energy of life. It is this one compound that allows for your body to perform so many functions in the blink of an eye. So, it’s pretty important!

Let’s look at exactly how your body does this.

“Beta” and “Oxidation” – What Does This Mean?

Example of a beta-carbon

==> The word, beta (β), implies the 2nd carbon removed from the “functional group” in a carbon chain. The 1st carbon is called the α-carbon.

(There is an example to the right. Here the functional group is the double-bonded oxygen.)

==> The word, oxidation, means that an oxygen is attached at that location. It is pulling electron density away from the β-carbon.

(So, imagine the same double-bonded oxygen on the β-carbon. This is what happens in beta-oxidation of fatty acids.)

So all of this “beta-oxidation” talk simply means your body is attaching a double-bonded oxygen 2 carbons down the line.

Example With Our Acyl-CoA[11]


Our acyl CoA is a long carbon chain (“R”) with a double-bonded oxygen and a coenzyme A attached at the end.

That “R” is representative of a long carbon chain. Your body will oxidize that β-carbon (where the “R” is sitting).

After it is oxidized, another coenzyme A comes to take the place of the entire right side of the molecule.

It steals the seat of the α-carbon. That means the whole right side of the original molecule (carbon + double-bonded oxygen group + coenzyme A group) has “fallen off.”


Everything to the right of the “R” is replaced by another coenzyme A group. The replacement causes an “acetyl-CoA” to fall off.

This is how your body generates that acetyl-CoA! Check out the picture to the right.

So afterwards, there is a shorter (by 2 carbons) fatty acid acyl-CoA and an acetyl-CoA.

Imagine the same starting molecule — now with a shorter “R” group + 1 acetyl-CoA (that fell off).

If we started with an 16-carbon saturated fatty acid, we now have a 14-carbon fatty acid with an acetyl-CoA.

Diagram of the first 2 rounds of beta-oxidation

So this keeps happening down the line until your body takes care of all the carbons.

The nature of the β-carbon being 2nd down the line each time makes it easy to keep track of the products.

The process creates half as many acetyl-CoAs as there are carbons in the starting chain.

Your body forms 8 acetyl-CoAs from a 16-carbon fatty acid.

Beta-oxidation occurs 7 times total in this example. The 7th run occurs on the last 4-carbon chain, so the result is 2 acetyl-CoA.

Important Side Products

At this point, we’ve gone through the overall process. Your body breaks down fatty acids. The result of this break down is a lot of acetyl-CoA. This acetyl-CoA will enter the Krebs Cycle (just like it does in the catabolism of glucose).

But before it does that, let’s get into a little more detail with the beta-oxidation reactions. With each loss of 2 carbons, there are actually multiple reactions that take place. It does not happen with one fell swoop.

Every time an acetyl-CoA falls off, 4 main reactions happen – involving 4 enzymes. These reactions create an awesome tool for our body. They generate FADH2 and NADH. These are the “electron transporters” that help generate ATP later in the process.

Beta Oxidation of a fatty acid

The four enzymes[10] acting on the acyl-CoA are:

1) acyl-CoA dehydrogenase

2) enoyl-CoA hydratase

3) hydroxy acyl-CoA dehydrogenase

4) ketoacyl-CoA thiolase

These enzymes act on the fatty acid one step at a time. When they’re all done, that’s when we see the shorter acyl CoA.

We will not go into detail with each step. We provide a diagram to the right if it interests you.

But we do want to focus on the main products of these intermediate steps:

  • 1 FADH2 with each cycle of beta-oxidation
  • 1 NADH with each cycle

Your body creates these with every run of beta-oxidation. But remember, there are only 7 total cycles of beta-oxidation for a 16-carbon fatty acid.

Likewise, a 14-carbon fatty acid goes through 6 cycles. It is half the chain length minus 1 (because of the last oxidation step).

Krebs Cycle and Electron Transport Chain

Let’s tally up our 16-carbon saturated fat:

  • 8 acetyl-CoA
  • 7 FADH2
  • 7 NADH

Not bad for this little fatty acid.

Krebs Cylce / Citric Acid Cycle / Tricarboxylic Acid Cycle


But it is not finished yet! These products are only another step in the direction of generating ATP.

ATP is the end goal – it is energy. It is how we live. At this point in the process, nothing is unique to fat metabolism (other than the amounts).

Both glucose and fat generate acetyl-CoA, FADHand NADH.

Each acetyl-CoA then goes on to the Krebs Cycle (shown to the left).

This cycle generates more FADH2 and NADH (electron transporters) with a small amount of ATP.

The FADH2 and NADH go on with the ones produced in beta-oxidation to the electron transport chain.

With each acetyl-CoA, you get: 1 FADH2, 3 NADH, and 1 ATP.

The electron carriers are the main result from this cycle because they generate so much more ATP in the electron transport chain.

Electron transport chain diagram

1 FADH2 generates about 1-2 ATPs in the transport chain.

1 NADH generates about 2-3 ATPs in the transport chain.

It starts to really add up when you think about it. This was from just one acetyl-CoA.

Remember, we have 7 more to go through from this one fatty acid chain!

That’s pretty amazing!

Because of how much common knowledge there is around the topic of the Krebs Cycle and the electron transport chain, we do not go into too much detail.

Most textbooks go through this stuff really in-depth if you so desire to learn. It is pretty cool stuff!

But we want to focus on the stuff that is not-so-common knowledge. Processes that you aren’t necessarily taught in school – like the beta-oxidation of saturated fat.

So, the main takeaways for these last two steps are:

  • Electron carriers (FADH2 and NADH) are generated and then used in the electron transport chain.
  • The electron transport chain is where most of the ATP generation occurs.
  • Fatty acids create a lot more acetyl-CoA than glucose does, so it creates a lot more ATP in the end.

Final Tally

So after all of this biological processing, what is the really the outcome? Great question! Let’s take a look!

The 16-carbon fatty acid (before the electron transport chain) creates:

  • 8 acetyl-CoA
  • 8 ATP (1 from each acetyl-CoA in the Krebs Cycle)
  • 15 total FADH2 (from both beta-oxidation and the Krebs Cycle)
  • 31 total NADH

Saturated Fat vs Carbohydrate

The end ATP production from 1 fatty acid chain: ~110 ATP!

Let’s compare that to 1 molecule of glucose: ~38 ATP.

The difference is huge! It is a complex process, but now you can see why fat is considered more “energy dense.”

This is also why you don’t need to eat as much on a high fat diet.

Whew! That was a long process. We are so impressed that you made it all the way through.

We hope this is helpful to you as a resource if anyone questions how your body is able to break down saturated fat.

This is just one step in the direction of proving saturated fats to be good. They have been demonized for too long. It’s time to bring them back.

And the best place to start was how your body breaks them down.


[1] Campbell NA, et al. (2017). Campbell Biology in Focus. Pearson Education Limited.

[2] Hamosh M, Scow RO. (1973). Lingual Lipase and Its Role in the Digestion of Dietary LipidJournal of Clinical Investigation 52(1): 88–95

[3] Liao TH, Hamosh P, Hamosh M. (1984). Fat Digestion by Lingual Lipase: Mechanism of Lipolysis in the Stomach and Upper Small IntestinePediatric Research 18(5): 402–409.

[4] Abrams CK, et al. (1988). Gastric Lipase: Localization in the Human StomachGastroenterology 95(6): 1460–1464.

[5] Yesiloglu Y, Kilic I. (2004). Lipase-catalyzed esterification of glycerol and oleic acidJournal of the American Oil Chemists Society 81(3): 281–284.

[6] (2018). PDB-101: Serum Albumin. [online] Available at: Accessed: 29 Mar. 2018.

[7] Schwenk R, Holloway G. (2010). Fatty acid transport across the cell membrane: Regulation by fatty acid transporters. Prostaglandins, Leukotrienes and Essential Fatty Acids 82(4-6): 149-154.

[8] Storch J, Mcdermott L. (2000). Fatty Acid Binding Proteins and Fatty Acid TransportCellular Proteins and Their Fatty Acids in Health and Disease 1486(1): 119–133.

[9] Campbell SE, et al. (2004). A Novel Function for Fatty Acid Translocase (FAT)/CD36Journal of Biological Chemistry 279(35): 36235–36241.

[10] (2018). Fatty Acid beta-Oxidation – AOCS Lipid Library. [online] Available at: Accessed: 29 Mar. 2018.

[11] (2018). Chapter 16 : Oxidation of Fatty Acids. [online] Available at: Accessed: 29 Mar. 2018.

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