Ah, these are always fun threads. Just spent an enjoyable hour I didn't really have studying up.
Becomiongoverweight, I'm curious about the mechanism of insulin response --> VAT uptake of stearic acid. As I've learned it, insulin causes cells to take up glucose, not fatty acids. But my knowledge is pretty limited.
Interestingly, when trying to search for what happens to dietary stearic acid, I found a study that suggests that stearic acid causes VAT apoptosis and death of adipocytes; in other words, stearic acid reduces VAT by killing VAT cells. Not sure if that's a good or bad thing. journals.plos.org/plosone/article
In that study, the mice were fed a roughly isocaloric diet. So maybe stearic acid ---> reduced VAT only when the we're *not* consuming excess calories.
Another possibility of not losing VAT on stearic acid: buildup of fat in liver. Apparently, in hypercaloric diets, dietary fatty acids accumulate in the liver, reducing its functionality. journals.plos.org/plosone/article
So perhaps some VAT reduction is occurring, but it is obscured by accumulation of fat in the liver. Though I imagine not--that would be several pounds of difference.
My general understanding of aiming for SAT gains over VAT gains--from a health perspective--is that SAT is less associated with metabolic syndrome and diabetes. Here's my general understanding of the process, based on articles I read years ago that I don't have the time to search for again rn, but will try to find when I have time:
1. The common explanation/narrative of adipose cells given in many health classes is wrong. The typical story is that you have a certain number of fat cells, and they expand indefinitely. You don't gain or lose fat cells with weight gain/loss; rather, fat cells expand or shrink according to triglyceride storage. This narrative is true, but only to a point.
2. In reality, adipose cells can't expand infinitely. Eventually, if too full of stored triglycerides, they burst.
3. The burst leads to an immune response cleanup crew of the burst cells, ie inflamation.
4. The immune response/inflammation signals nearby adipose cells to decrease insulin sensitivity so that they don't succumb to the same fate. In other words, insulin resistance is an adaptive response to overburdened adipose cells.
5. An alternative adaptive response to a high need for triglyceride storage AND to insulin resistance would be adipogenesis or adipose hyperplasia--the growth of additional adipose cells, to spread the burden of triglyceride storage.
6. I remember reading a mouse study years ago in which some gene was knocked out that limited adipogensis. Mice with insulin resistance and metabolic syndrome grew new fat cells, gained weight, AND were cured of metabolic syndrome and insulin resistance. Growing new adipose cells seems to be the golden ticket for gaining.
7. For some reason, SAT has a limited ability to increase the number of cells in hypercaloric diets, while VAT seems to maintain a set number of cells.
So if the overburdened adipose tissue hypothesis is correct, I'm not sure killing off VAT cells is the way to go.
Of course, my understanding could be entirely wrong. I'm no expert. It's just been what I've been able to piece together from articles I found (as well as articles you've shared over the years).
Becomiongoverweight, I'm curious about the mechanism of insulin response --> VAT uptake of stearic acid. As I've learned it, insulin causes cells to take up glucose, not fatty acids. But my knowledge is pretty limited.
Interestingly, when trying to search for what happens to dietary stearic acid, I found a study that suggests that stearic acid causes VAT apoptosis and death of adipocytes; in other words, stearic acid reduces VAT by killing VAT cells. Not sure if that's a good or bad thing. journals.plos.org/plosone/article
In that study, the mice were fed a roughly isocaloric diet. So maybe stearic acid ---> reduced VAT only when the we're *not* consuming excess calories.
Another possibility of not losing VAT on stearic acid: buildup of fat in liver. Apparently, in hypercaloric diets, dietary fatty acids accumulate in the liver, reducing its functionality. journals.plos.org/plosone/article
So perhaps some VAT reduction is occurring, but it is obscured by accumulation of fat in the liver. Though I imagine not--that would be several pounds of difference.
My general understanding of aiming for SAT gains over VAT gains--from a health perspective--is that SAT is less associated with metabolic syndrome and diabetes. Here's my general understanding of the process, based on articles I read years ago that I don't have the time to search for again rn, but will try to find when I have time:
1. The common explanation/narrative of adipose cells given in many health classes is wrong. The typical story is that you have a certain number of fat cells, and they expand indefinitely. You don't gain or lose fat cells with weight gain/loss; rather, fat cells expand or shrink according to triglyceride storage. This narrative is true, but only to a point.
2. In reality, adipose cells can't expand infinitely. Eventually, if too full of stored triglycerides, they burst.
3. The burst leads to an immune response cleanup crew of the burst cells, ie inflamation.
4. The immune response/inflammation signals nearby adipose cells to decrease insulin sensitivity so that they don't succumb to the same fate. In other words, insulin resistance is an adaptive response to overburdened adipose cells.
5. An alternative adaptive response to a high need for triglyceride storage AND to insulin resistance would be adipogenesis or adipose hyperplasia--the growth of additional adipose cells, to spread the burden of triglyceride storage.
6. I remember reading a mouse study years ago in which some gene was knocked out that limited adipogensis. Mice with insulin resistance and metabolic syndrome grew new fat cells, gained weight, AND were cured of metabolic syndrome and insulin resistance. Growing new adipose cells seems to be the golden ticket for gaining.
7. For some reason, SAT has a limited ability to increase the number of cells in hypercaloric diets, while VAT seems to maintain a set number of cells.
So if the overburdened adipose tissue hypothesis is correct, I'm not sure killing off VAT cells is the way to go.
Of course, my understanding could be entirely wrong. I'm no expert. It's just been what I've been able to piece together from articles I found (as well as articles you've shared over the years).
2 years
