What happens to those fat cells?


Have you seen this Review article from2018? It is also frustrated by the lack of knowledge in this area, but some of the techniques and references they provide might be of help.

Therefore, despite the broad acceptance of the adipose expandability hypothesis, there is a scarcity of data to describe the in vivo dynamics of adipose turnover and the link with metabolic health in humans. Early studies proposed that adipocytes are produced only during childhood and adolescence [29] but in vivo evidence is necessary to substantiate adipocyte generation in adulthood. Below, we review two novel and distinct in vivo approaches that have been implemented in humans.

(Karim Wassef) #62

Thank you. Yes! I come across this idea that adipose cell count is set during childhood and adolescence and can’t be changed… but I couldn’t find any evidence.


And this one from 2008 may or may not be included in that review…

(Kirk Wolak) #64

So I have a good friend who is big and fluffy fat.
Amazingly at 60 y/o and lifelong obesity, he does not have high glucose (no diabetes).

But he gains fat VERY easily. so… In his case, overeating leads to storage/obesity, but the metabolic damage is not happening at the same speed. So I tend to disagree that metabolic damage causes obesity (as the ONLY cause). Unless you consider being a good fat storer to be metabolic damage, which I don’t.

So, it appears we have:

  1. Normal metabolism, healthy weighted people not DRIVEN to eat
  2. Abnormal metabolism people who become IR and that drives obesity and T2D, etc
  3. TOFI who appear to store the fat in the liver
  4. FLUFFY who appear to store the fat in their non-liver fat cells

And there are probably many descriptions of #4 including my old noon aid, who had the gigantic hips/thighs and this little torso. Those fat cells were probably very sensitive to insulin. Others, not so much…

(Karim Wassef) #65

Actually, some people have the “gift” of being able to add more subcutaneous adipose cells for more fat storage… they’re not limited like the rest of us.

With more fresh fat cells being made, they don’t suffer from overstuffed fat cells and high insulin and glucose…

While we’re trying to stuff our freezers… they just make more freezers.

(Kirk Wolak) #66

I like that as an example.

So, we have people who can:
A) Grow the number of fat cells (probably in a specific body part: Liver, Legs, belly, everywhere)
B) Overstuff their fat cells (because they can keep stretching)
C) Become Insulin Resistant (not enough creation, not enough stuffing)
D) Hit a trigger point (Epigenetics) that triggers A and/or B after too much C.

Wow, I bet we will discover a genetic marker for this that indicates this.

And that is a Hypothesis that makes sense to me. It covers a concept of individual response to stimuli that we would need to keep evolving in a world of changing demands…


This is known as lipidemia. I believe my mother had this disorder and it caused her edema in the legs and ankles too. I didn’t inherit it, but got an apple shape from my T2D father instead.



Where else can you ask a “simple” question and learn so much?

(Mame) #69

Is it? I am not so sure about this. Except for unfertilized eggs stored in ovaries doesn’t every single cell have a life span that is shorter than the body’s life span? That means they have to be cleaned up after they die. although perhaps some like fat cells are automatically replaced one for one.

This does make sense to me in that one’s fat storing capability remains fairly constant, although I would posit that for women it changes with age. (maybe) Post menopausal one would not need the same amount of fat stores to protect the next generation. I hope that our body is smart enough to know this. Why waste resources creating fat on thighs and bum one no longer needs… Something to look forward to as I get older! :slightly_smiling_face:


(Ethan) #70

That is exactly correct. The body replace the cell with another.

(Mame) #71

I believe this is what we think happens but I have not seen this proved…it’s a reasonable theory but then 20 years ago everyone was sure new brain cells weren’t made after age 25…

(Ethan) #72

Yes that is true. It is based on evidence, but not complete evidence.


Ahhh… good to know that, thanks!


There is also a lot of fluid loss with glycogen from the liver and reduced inflammation of the fat lining the digestive tract. It may be difficult to measure inside organs and the actual fat loss compared to the reduction of ‘fat mass’ which includes supportive tissue and fluid.

But yes, the triglycerides inside the liver should be used rapidly when conditions allow compared to peripheral tissues.

(Bacon by any other name would taste just as great.) #75

Dr. Robert Lustig says that the medical literature distinguishes between the obese with metabolic damage and the MHO (metabolically-healthy obese), who are perfectly healthy, with completely normal metabolic markers. The latter apparently make up about 20% of the obese population.

The reverse situation is lean people, who are generally healthy, but 30% of whom are just as metabolically deranged as we usually assume the obese are. These 30% look lean but are riddled with viseral fat, and one researcher coined the now-standard term TOFI for them: “thin on the outside, fat on the inside.”

So you are quite right to say that obesity and metabolic derangement are by no means the same thing.

(Bunny) #76

Granted we are not a mouse or rat, that’s what they might be finding in knock out mice and rats that are humanized with the 48 hour fasting and 25% loss in visceral fat or they reached this conclusion on actual human beings?

The article on this suddenly disappeared from the endocrinology journal I was reading or I am just having trouble tracking it down, I swear I bookmarked it twice and it’s now gone?


Happens to me all the time!

(DougH) #78

Hard to know short of a muscle biopsy, and that is a nope from me.

Strength is a combination of many things, but hypertrophy is definetly one of the legs of the stool. As you do any resistance training some strength gains are form and some is neurological capacity, but you eventually top out at some individualized level without introducing hypertrophy.

If you weren’t giving your body signals to preserve your leg muscle it very well may have decided that was an area that could have been given up for some protein.

(Nasir) #79

I have a feeling I am in this group. Very large thighs, subcutaneous fat on/around belly, arms and under arms etc. Normal BG (A1C is 5.2), normal BP, normal lipids. Fairly active (longest bike ride 60KM+, longest walk 12KM+ etc despite being morbidly obese, 350+lbs now down to 305lbs)
Any other “symptoms” of being in this group? Any suggestions for weight loss for this group other than KCKO?

(Bacon by any other name would taste just as great.) #80

Dr. Phinney advises people who are feeling stuck to cut their carbohydrate even further. If that doesn’t work, he says, eat more fat. On no account, he says, should you increase your carb intake.

Some carnivores say that going carnivore was the only thing that helped them lose weight.