Dietary Lipids and Your Mitochondria

Dietary Lipids and Your Mitochondria

Your Mitochondria and Diet

So what’s up with your mitochondria? Are they doing alright? Or are they generating ROS and leaking protons?…

What the heck does that even mean?? We will be diving into all that later.

The research studied for this week was about dietary fats, calorie restriction, and problems with cellular processes.

The mitochondrion

Specifically, it was about how types of fat and quantities of fat affect your membranes.

Fat does not stay fat in your body. It changes after you eat it.

But after it goes through some manipulation, they are either used for energy or they contribute to your cellular make-up.

This is awesome – because it is those fats in the membrane that allow for life to occur. If you did not have fats as the material of your membrane, you would not survive.

But how much do you really need to eat to gain the benefits? And what kinds are best to keep you healthy?

When your membranes are made of the right stuff, you can experience life in a whole new, LONGER way.

We suggest that membrane integrity is correlated with certain problems of the mitochondria: ROS production and proton leak.

But are these membranes the direct cause of ROS (reactive oxygen species) production and proton leak? Right now, we do not know. But we do know there is a correlation.

These may seem like “big words”, but don’t worry. Just know that these things are bad in large amounts.

ROS production is when your mitochondria produce a compound that reacts and degrades parts of your cell. Proton leak occurs when your mitochondria do not want to produce any more ATP, or when you have malfunctioning proteins in the membrane.

Let’s take a look.

Summary of the Article:

  1. Calorie restriction leads to “better” mitochondrial membranes.
    1. Less unsaturated membranes, ROS production, and proton leak.
  2. The fat composition in the membrane does not correlate with ROS production.
  3. The fat composition does correlate with proton leak.
    1. Saturated fats produce the least amount.


Alright, so before we get started, here is the exact piece of research we are reviewing today:

==> The Influence of Dietary Lipid Composition on Skeletal Muscle Mitochondria From Mice Following 1 Month of Calorie Restriction (conducted by Yana Chen, et alia at the University of California, Davis). [1] 

[This Week’s Research File]

Lab mice

This research article had a few points of discovery, but the most significant finding was relating to proton leak. So that is our main focus, but understand we will be going into other topics as well.

Before we go too far, this study was conducted on mice only. This is one limitation of the study.

However, the professional community accepts studies done on mice are a good starting point for understanding how humans are affected.

Another limitation was that it only lasted one month. It was not a long-term study.

Ready? Let’s get started.

Experimental Approach:

The researchers fed 4 groups of rats 4 different meal plans.

  • A control group — soybean oil (95% of a typical 12.5 kcal/day diet).
  • Calorie restricted (CR soybean) — soybean oil (60% of control group diet at 8.6 kcal/day)
  • Calorie restricted (CR fish) — fish oil (60% of control group diet)
  • Calorie restricted (CR lard) — lard (60% of control group diet)

From these diets, the researchers looked at three main factors after 1 month:

  • membrane composition
  • ROS production
  • proton leak

For the sake of brevity, we will not go into exactly how these were measured. You can find this in the study itself. The procedures were all standard for this type of experiment.

The researchers wanted to look at these effects as a review of the membrane theory of aging.

Membrane Theory of Aging

Researchers set out to review the membrane theory of aging: “[I]t is the age-related changes of the cell’s ability to transfer chemicals, heat and electrical processes that impair it.” [2]

This boils down to basic biochemistry. The higher number of double bonds in a membrane, the more likely it is to break down from problems (like peroxidation). This leads to aging. Those highly double-bonded fats are called “polyunsaturated fatty acids” (PUFA).

That makes sense because double bonds are more reactive than single bonds.

Aging pathway of the mitochondria

So how do we reduce the double bonds (i.e. unsaturation index) of our membranes? There are many answers to that question.

But this study can confirm one thing: calorie restriction causes a significant reduction in the unsaturation index.

More specifically, it has been shown that calorie restriction decreases the PUFA percentage and the omega-3 (n-3) content of the membrane.

==> It is not clear here why the omega-3 composition, rather than the omega-6 composition, was analyzed. But that’s what we are working with in this study.

Having a lower PUFA percentage predicts a longer life by preventing peroxidation and oxidative stress. [3,4]. This should be our goal — to keep membrane integrity by reducing the number of double bonds.

This article goes into what exact membrane compositions affect aging problems, and what types of fats produce them.

The Problems:

So are unsaturation index, reactive oxygen species, and proton leak that bad? What do they really imply?

Here is a very quick, but summarized answer:

==> Unsaturation index is bad. It leads to peroxidation and damage. [1]

==> Reactive oxygen species production is bad in excess. These cause the stated damage to the unsaturated membranes. [1,2]

==> Proton leak is also bad in excess. Some is good. More is worse. It provides for a less efficient mitochondria. [5]

The question this study wanted to answer was if diets can change these factors. And they can! But our extent of understanding is limited.

Conclusions of the study:

The researchers looked to dietary fats to find correlations with the three main problems described above.

Unsaturation Index:

Different dietary fats did correspond to different membrane lipid composition. But the results themselves differ tremendously from other studies. We explain this more later on.

But for now, let’s look at their data.

The data results are presented below:

Table 5 - fatty acid composition of phosphatidyl choline (mitochondrial membrane)

Table 6 - fatty acid composition of phosphatidyl ethanolamine (mitochondrial membrane)Table 7 - fatty acid composition of cardiolipin (mitochondrial membrane)


That’s a lot of data. But the main takeaway is that your diet affects your membrane composition. Especially look at the circle data points.

Comparing to soybean oil, it looks like having a higher saturated fat diet (lard) creates more unsaturation in your membrane. This was true for 2 out of the 3 types of tissues looked at in this study.

Again, this goes against already established data. Dietary saturated fats cause less unsaturation in your membranes, while unsaturated fats cause more unsaturation. [6,7,8,9]

But you can also see on the tables there are data points that are not “significantly different.” Those would be the values with superscripted letters. There are a large amount of them. So most data between fats is not super useful.

A second look at the sources of fat would explain why there is a problem. Their “saturated fat source” was only 40% saturated fat with 60% unsaturated fat.

The previous studies (with more significant sources of saturated fat) are a better determination of how diet turns to membrane composition.

This being said, lard did still contain more saturated fat than the others in this study.

Take a look at the tables below for the food ingredients and fat compositions:

      Table 1 - Ingredients in mice foodTable 2 - fatty acid composition of food

But what data is useful then? A trend that calorie restriction caused less unsaturation. But even these data points are not significantly different from one another.

Compare the control soybean group to the restricted soybean group. In 2 out of 3 cases, the unsaturation index decreased.

ROS Production:

“The results from our study indicate that alterations in mitochondrial phospholipid fatty acid composition do not significantly influence H2O2 [ROS] production with CR regimens.”

Figure 1 - ROS production

So essentially — there was no determination of how dietary fats, membrane composition, and ROS production are related.


They did find something. Your mitochondria will produce less ROS from having a restricted diet. This means that eating less can help your mitochondria from being peroxidized.

So – there was no difference in ROS production between the types of fats. But there was a difference in ROS among the amount of fat.

Proton Leak:

There were 2 obvious trends in the amount of proton leak:

  • Calorie restriction decreased proton leak
  • Lard consumption decreased proton leak (significantly more than the other fats)

Figure 2 - proton leak

Take a look at the graph. The lard group is in the upper left corner. That means it produces more electric potential (less proton leak). The mitochondria were more better at keeping a proton gradient. They were not losing energy.

Eating saturated fat is more efficient and generates less proton leak.

Main Takeaways?

There is so much more to talk about in this blog post. But we cannot talk forever. The study goes into much more detail about certain topics that we decided to only summarize.

While that might have seemed dense, we want to show it’s just a bunch of large data and words. We don’t want to intimidate you. We can boil down this study to 3 conclusions:

  • Calorie restriction on a fat-diet is good.
    • It lowers the unsaturation index, lowers the ROS production, and lowers the proton leak.
  • The types of fats in a membrane do not determine ROS production.
  • The types of fats do determine proton leak.
    • Saturated fats are the best with the smallest amount of leak.

Now, we want to reiterate this is just one study. It does not give the whole picture. Also, much of the data was not significantly different between types of fats.

But it at least gives us a starting point. We can use studies like this to understand how diet might affect your body (specifically, the mitochondria).

What you eat does make a difference to how your body works on a molecular level…

Make sure to keep the motor of your body working smoothly! Eat more fat as part of a ketogenic diet.


[1] Chen, Y. et al. 2012The Influence of Dietary Lipid Composition on Skeletal Muscle Mitochondria From Mice Following 1 Month of Calorie RestrictionThe Journals of Gerontology: Series A. 671121–1131.

[2] Walker, W. and Pagare, V. 2018. Theories of Aging. [online]. Physiopedia. Available at: Accessed: 26 Mar. 2018.

[3] Laganiere S, Yu BP. 1993. Modulation of membrane phospholipid fatty acid composition by age and food restriction. Gerontology. 39: 7 – 18.

[4] Faulks SC, Turner N, Else PL, Hulbert AJ. 2006. Calorie restriction in mice: effects on body composition, daily activity, metabolic rate, mitochondrial reactive oxygen species production, and membrane fatty acid composition. The Journals of Gerontology: Series A. 61(8): 781 – 794.

[5] Brand, M. D., Chien, L.-F., Ainscow, E. K., Rolfe, D. F. & Porter, R. K. 1994. The causes and functions of mitochondrial proton leakBiochimica et Biophysica Acta (BBA) – Bioenergetics 1187(2)132–139

[6] Geiser, F. 1990. Influence of polyunsaturated and saturated dietary lipids on adipose tissue, brain and mitochondrial membrane fatty acid composition of a mammalian hibernatorBiochimica et Biophysica Acta (BBA) – Lipids and Lipid Metabolism 1046: 159–166.

[7] Mcmurchie, E. J., Gibson, R. A., Charnock, J. S. & Mcintosh, G. H. 1986. Mitochondrial membrane fatty acid composition in the marmoset monkey following dietary lipid supplementationLipids. 21(5): 315–323.

[8] Guderley, H., Kraffe, E., Bureau, W. & Bureau, D. P. 2008. Dietary fatty acid composition changes mitochondrial phospholipids and oxidative capacities in rainbow trout red muscleJournal of Comparative Physiology B 178(3): 385–399.

[9] Schenkel, L., Bakovic, M. 2014. Formation and Regulation of Mitochondrial Membranes. International Journal of Cell Biology 2014: 1-13.

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