What happens to those fat cells?


#1

SO I have always been taught that even if you lose a lot of weight your existing fat cells simply shrink. Even if we lose some fat cells each year (8% is bandied about) the absolute number is more or less fixed in early adolescence. Anybody know what happens in long-term ketosis? Do the fat cells just shrink and hang around or do they gradually go away?


(Boots on? Balls to the wall? Good start.) #2

Seems it varies from person to person. Gabor Erdosi has a lot of info on the issue - worth a google.


(Carl Keller) #3

According to proponents of the whoosh effect, when our fat cells shrink, they fill up with water. This might explain how we can often lose fat and inches, but not show it when we step on a scale. Eventually, if conditions are right, the water in those fat cells is flushed and a dramatic loss can be noted on the scale.

In adults, fat cells may die but they get replaced with new fat cells. Fat cells are a normal part of our physiology. The problem is when we ask them to do too much.

https://well.blogs.nytimes.com/2017/02/17/are-fat-cells-forever/


#4

I doubt they go away and it wouldn’t be a good idea if they did. It’s the small, healthy fat cells that store and release energy as you need it. If you could somehow (let’s say surgically) remove fat cells, it would make a person metabolically less healthy.

The water people store “in” fat cells is more likely inflammation of tissues surrounding fat cells. Take away the cause of inflammation, and the swelling goes down releasing fluid.

The aforementioned Gabor talking about IR and overstuffed fat cells:

https://www.breaknutrition.com/episode-5-enlarged-adipocytes-overloaded-lipids-lead-insulin-resistance/


(Bacon is the new bacon) #5

The number of fat cells and the ability to make new ones is thought by some researchers to explain why some fat people don’t get metabolically ill (“MHO”—metabolically healthy obese) and some thin people do (“TOFI”—thin on the outside, fat on the inside). The idea is that the more ability one has to store fat without damaging the existing fat cells and making them insulin-resistant, the less likely accumulated fat will cause other problems. By this reasoning, TOFI’s develop metabolic disease because they reach the limit of their fat storage early.

Whether or not this is actually true, it’s an intriguing hypothesis. My only problem with it is the underlying assumption that obesity causes metabolic disease, whereas from what I have learned, it appears that obesity—like cardiovascular disease, diabetes, hypertension, gout, Alzheimer’s disease, etc.—is instead one of the consequences of metabolic disease (this is an idea I first encountered by watching Peter Attia’s TED talk). So it is addressing the underlying metabolic problem that cures obesity and all the other health problems.


#6

I’d say the obesity is still a symptom of an underlying cause that forced the adipose tissue into a state of overload. You can have excess insulin from food driving fat cells to fill up [edit: either from dietary fat eaten with a high insulin meal OR lipogenesis in the liver]. The more overstuffed and dysfunctional cells, the higher the IR. Downward spiral. It does look like the chicken and the egg.

Or, alternate hypothesis: the root of adipose dysfunction begins in the gut. Certain substances, like fructose and alcohol, cause an immune inflammatory response in the abdominal fat, which causes an inmmune and incretin cascade downstream. This also applies to refined carbs triggering microbiome disbiosis and “leaky gut”.


(Full Metal Keto) #7

Isn’t that what liposuction is? :cowboy_hat_face:


#8

Yes. I’ve seen some cryo-therapy ads on tv too. I can’t even begin to think about what it might do to the body to have a bunch of frozen-to-death fat cells sitting around.


(d043db25bf22d2e46dea) #9

Fascinating thoughts. I’m “skinny fat” and got myself into insulin resistance, high cholesterol and a cascade of problems by what appears to be eating fruits, drinking wine and having chocolate. I didn’t even eat grains or bread much, but I ate an insulin bomb of a breakfast: oatmeal with honey, fruits and sweet yogurt (washed down with a litre of coffee;)… and I grazed on fruits throughout the day… well a few years of this “healthy lifestyle” and I ended up with panic attacks, female hormones out of wack and prediabetis:(

I’m on week 2 of keto and the sugar is totally normal🙌 I also notice the fat shrinking around those "hard to get rid off " areas around my waist and thighs.

I wish they would teach us this stuff at school. So much unnecessary suffering due to sugar.


(Karim Wassef) #10

There’s also the inverse…

By taking mice that could not make fat cells, and therefore diabetic, and injecting them with fat cells… they were able to reverse the diabetes.

I need to find that video but it’s fascinating. The new cells were receptive and able to take in glucose… so the insulin resistance went away.

Basically: more storage space = less gunk = less disease.

Fat gets a bad rap but subcutaneous fat is not the bad guy. It’s coming in to clean up the mess. Like cholesterol, it’s a good guy.


(Carl Keller) #11

Deception is more profitable than truth.


(Bacon is the new bacon) #12

You can also prevent diabetes in mice by taking away their ability to make glucagon.

We don’t need no stinkin’ fat cells!


(Karim Wassef) #13

?? That one’s new to me.

Why would not having glucagon fix diabetes?

If you’re at your genetic limit for fat cells, & you can make them take any more glucose… you become insulin resistant.

I would think glucagon would help empty them and allow for more storage later?


#14

This makes sense. Those of us that are obese without any significant markers of metabolic disease, probably got that way because of imbalance rather than full-blown disease.


#15

Maybe they were specially breed diabetic mice with glucagon resistance? So they were getting glucose in their food plus not being able to shut down lipolysis at the same time, which leads to high blood glucose.


(Bacon is the new bacon) #16

As I understand it, the hypothesis is that glucagon is the primary regulator of gluconeogenesis, with insulin along merely to act as a brake on the system. Glucagon will run riot in the absence of insulin, but when both glucagon and insulin are absent, it appears that other mechanisms still regulate the level of serum glucose.

I don’t claim to understand this entirely, or to be entirely convinced, for that matter, but it is part of the current speculation about what is actually going on, and I believe that this kind of fresh thinking, whether ultimately proved right or wrong, should be encouraged.

Malcolm Kendrick discusses this in a blog post:


(Bunny) #17

My thoughts on this:

Having more body fat does not make us fat, it is what’s being stored (lipids/glucose) inside the adipose fat cell and thus becomes more of an inflamed receptor than a transmitter because it is storing excess energy or more energy than is being used?

Fat cells can act like swelled up storage tanks, so the more your body will work to defend that equilibrium (depending on how fat you are) or what ever equilibrium you are trying to maintain.

If you can get the mitochondria (what is building and feeding the fat cell to begin with) outside the lipids inside the fat cell to free float in the cytoplasmic fluid within the adipocyte, like what happens with cold thermogenesis exposure in brown fat, then you burn up the lipids and/or glucose for energy immediately through a heat generating mitochondrial process called UCP-1; a process where it becomes more electrical than chemical.

Ketosis actually empties the extra lipids floating around with the cytoplasmic fluid inside the fat cell, so we actually DO NOT lose fat cells, we lose the lipid droplets inside the fat cell which are replaced with more cytoplasmic fluid than lipid droplets, even if you try to surgically remove fat cells or kill them they will come right back and make larger fat cells to make up the difference when it starts the adipogenesis process all over again from left over stem cells.

Note: I am using the term fat cell, adipose or adipocyte tissue interchangeably because this type of tissue does not have to necessarily contain lipid droplets/fat.


(Karim Wassef) #18

I guess the question is… does autophagy remove the empty fat sacs permanently or do they do come back (still empty), even without a caloric or hormonal stimulus?

I have to actively weight train to rebuild muscle lost during fasting. What triggers the regeneration of the empty adiposites, if they’re regenerated at all?

I think that they do… based on my n=1


(Bunny) #19

Eating too much sugar and/or fat (that is then turning to sugar) and/or eating too much meat that is turning to sugar. Sugar always turns (converted) into fat/lipids if you are taking in more than you are burning (energy expenditure). Once glycogen stores are replenished and your using more glucose than ketones or FFA’s for energy.

Fat cells (as they are called) don’t “empty” they should be small and healthy and contain some lipids/fat but more cytosol than lipids/fat.


(Karim Wassef) #20

So if there is no surplus, does the body regenerate those cells post - autophagy?