Bigwideland:
I have been reading up on the development of fat cells. Most articles conclude that you can increase the number of fat cells to about 23 or 24 but most in adolescents year's. These tend to be cells under the skin. These can increase is size without much metabolic risk.
Once you are over 25 your fat cell counts are mainly unchanged. So you can gain till you Max out your cell capacity with low metabolic issues. After that your increase in weight is in your organs like your liver ect. This can lead to diabetes and so on.
So that explains to some degree how some people get to huge size as adults they developed more cells as teenagers.
Do we have any expert's that can input on this.
And how, if true can you know you maxed out your fat cells capacity?
I have been reading up on the development of fat cells. Most articles conclude that you can increase the number of fat cells to about 23 or 24 but most in adolescents year's. These tend to be cells under the skin. These can increase is size without much metabolic risk.
Once you are over 25 your fat cell counts are mainly unchanged. So you can gain till you Max out your cell capacity with low metabolic issues. After that your increase in weight is in your organs like your liver ect. This can lead to diabetes and so on.
So that explains to some degree how some people get to huge size as adults they developed more cells as teenagers.
Do we have any expert's that can input on this.
And how, if true can you know you maxed out your fat cells capacity?
Not an expert, but the search term you’re looking for is “adipose tissue hyperplasia”—that means increasing the number of fat cells. Sometimes helps to include specifiers like “white adipose tissue hyperplasia” or “subcutaneous adipose tissue hyperplasia”. (“Hypertrophy” means filling up those fat cells)
There was a neat paper from… close to a decade ago? 2015 maybe? That used a mouse model to first induce obesity with a high fat diet, and then cure it by using a hormone cocktail to induce hyperplasia.
The mice gained weight after the cocktail, but the size of the cells was smaller; they reversed the hypertrophy by inducing hyperplasia, giving the mice more room to store fat (ie, there was somewhere for the blood sugar to go. No more systemic insulin resistance or diabetes).
These results seem consistent with some conclusions about “metabolically healthy obese” (MHO) humans, who typically have smaller and more plentiful fat cells.
A fairly comprehensive paper I read in… 2018? Addressed a lot of evidence that the systemic insulin resistance of T2DM is a result of fat cells becoming too hypertrophic and bursting, signaling to others to become insulin resistant.
I really do have to collect these papers in a sensible place at some point lol.
9 months
