Want “hotter” fat cells? Change your diet!
As you know, I’m a scientist that studies cellular metabolism. In recent years, my lab has focused on understanding variables that influence the metabolic rate in fat cells. What we’ve found, across isolated fat cells, as well as fat tissue from rodents and humans, is worth highlighting.
The primary part of the cell that is responsible for “burning” fuel to create “energy” is the mitochondrion (singular). When the mitochondria (plural) are doing their job, they take in molecules from glucose, fats, and ketones and turn them into ATP, which is the molecule that the cell uses to work and perform its duties in the body. ATP is sometimes just referred to as “energy”–it’s the currency the cell uses to purchase work. For example, when a neuron sends an electrochemical signal, it uses ATP to get it done. When a muscle contracts and relaxes, it uses ATP to get it done. This occurs in all cells in countless unique ways.
Burning fuel and making ATP are two halves of a whole–they usually occur synchronously–a cell will burn enough fuel to make a required amount of ATP. In other words, it’s demand-driven. We call this efficient process “coupled”–fuel use is coupled to ATP production–like a ratio of 1:1. This ensures the cells aren’t wasting fuel.
In some instances, the mitochondria become “uncoupled”–they begin burning more fuel than they should based on the amount of ATP the cell is demanding. It’s as if the cell is asking for 1 molecule of ATP to get some work done, but the mitochondria burns 2 units of fuel; the normally coupled and efficient process becomes uncoupled and less efficient, like a ratio of 2:1.
This excess fuel burning, the uncoupled state, results in a higher metabolic rate (after all, the mitochondria are burning much more fuel) that simply results in greater heat production. Because of this, it’s no surprise that mitochondrial uncoupling is a good way for a body to make more heat and, thus, it occurs more with cold exposure.
We actually have small pockets of a fat that is specifically designed to do this, called “brown fat”. In humans, our brown fat largely exists in small areas throughout our rib cage. However, the majority of the fat we have is called “white fat”–it’s literally white-ish because it has so few mitochondria, which is a stark contrast to the brown fat, which is dark reddish-brown color due to high prevalence of mitochondria. Remarkably, under the right circumstances, our white fat, and its very low metabolic rate, can begin to behave like brown fat, with its high, uncoupled metabolic rate. That’s where my research comes in.
In 2018, my lab published our first findings on this topic.  We used laboratory mice to test the effects of insulin on altering mitochondrial function in white and brown fat tissue. As I mentioned above, brown fat has a high metabolic rate because of its highly uncoupled mitochondria. Insulin treatment in the animals dramatically slowed this effect–it essentially made the brown fat behave more like white fat. In contrast, the insulin treatments had no effect on white fat–the low-rate, coupled mitochondria were just as slow and content as they ever were.
These results are a stark contrast to our second study. This time, we went beyond using just laboratory mice to include both isolated fat cells and human fat tissue. At first, we grew fat cells in little petri dishes and incubated/fed them with ketones (remember, ketones can only be made in the body when insulin is low) and found that the mitochondria became much busier and more uncoupled (i.e., higher metabolic rate). Moreover, in the mice, the higher ketones did the opposite of what insulin did in the first study–the brown fat was as busy as ever, but this time the ketones stimulated the white fat to behave more like brown fat. Basically, the ketones were stimulating the white fat almost like cold exposure does! The cherry on top was confirming the same effect in humans. We had people come into our lab that were following either a standard or ketogenic diet and performed a fat biopsy to remove a small piece of fat in their bellies. Upon testing, we found that the fat tissue metabolic rate from people in ketosis was about 2-3X higher than the other group.
Recently, we again confirmed these findings, but this time in a long-term study.  By collaborating with a group at Harvard, we were able to test the fat tissue mitochondrial metabolic rate in people before and after following a diet for 12-15 weeks. The study subjects were assigned to one of three dietary groups for those weeks, with the groups differing in the balance of carbohydrate to fat. The group that ate the highest amounts of carbohydrates (60% of calories) had no change in fat cell metabolic rate. Both of the other groups (40% and 20% carbohydrate) had a significant increase in fat cell metabolic rate.
In the average person, fat tissue accounts for about 5-10% of whole-body metabolic rate in humans.  This means that lowering insulin and increasing ketones could have a whole-body metabolic benefit and even partly explain why metabolic rate increases when insulin is low.  Whatever the total effect, there’s no doubt that fat tissue has a metabolic rate that can be altered depending on what we eat and how hormones respond to those foods.
This article is for informational and educational purposes only. It is not, nor is it intended to be substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.