Studies? Where Is Evidence PUFAs Are Preferentially Stored Not Burned?

[Luann]

Does anyone know whether the fat created via lipogenesis tends to be saturated or unsaturated?

Any fat that's made through de novo lipogenesis from carbohydrate will be saturated.

I thought it was about the ratio of saturated/ unsaturated. Hence, the frying out the fat in bacon or chicharrones and refrying in coconut oil, cooking eggs in coconut oil, or adding coconut oil to peanut butter.

If PUFA is that much harder to burn then the body's ratio of saturated / unsaturated will ALWAYS be lower than the diet ratio. It is really about the total amount of PUFA or more specifically about the body ratio of SFA / UFA.

 

[Dante]

I just googled the changes to adipose composition after fasting. From some studies it looks like the PUFA is quick to get liberated but then it concentrates in the fat cells. So it is not burned. In fact the fat tissue after fasting has a higher linoleic acid to SFA ratio which means that less saturated species of fat are getting lost through fat burning.

The abstract of this paper says otherwise
Selective mobilization of adipose tissue fatty acids during energy depletion in the rat. - PubMed - NCBI

 

[lvysaur]

In fact the fat tissue after fasting has a higher linoleic acid to SFA ratio which means that less saturated species of fat are getting lost through fat burning.

Don't you mean that more saturates are getting lost?

Additionally, there's a bit of a contradiction in the thread subject; I remember reading about PUFAs getting processed more quickly than saturated fats.

 

[Luann]

Yep that's what I meant.

Interesting @Dante. Here are the studies I was looking at that showed the fat composition becoming less saturated.

Preferential retention of linoleic acid-enriched triacylglycerols in liver and serum during fasting

Fasting-induced selective mobilization of brown adipose tissue fatty acids

 

[ecstatichamster]

I think this is a landmark study:
Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver

It's a mouse study.

1. Mice given fatty diets incorporate the fat basically as-is into liver and tissue
2. Soy oil caused diabetes
3. Fructose even with soy oil PROTECTED against diabetes
4. Coconut oil was NOT causing diabetes.

It is an amazing study.

And this one sheds light on this thread:
Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC507283/pdf/972081.pdf

Subjects (humans) given high fat or high sugar diets and monitored for a few weeks.

By day 10, VLDL triglyceride was markedly enriched in palmitate and deficient in linoleate in all subjects on the low fat diet.

Newly synthesized fatty acids accounted for 44 +/- 10% of the VLDL triglyceride.

Mass isotopomer distribution analysis of palmitate labeled with intravenously infused 13C-acetate confirmed that increased palmitate synthesis was the likely cause for the accumulation of triglyceride palmitate and "dilution" of linoleate.

In contrast, there was minimal fatty acid synthesis on the high diet. Thus, the dietary substitution of carbohydrate for fat stimulated fatty acid synthesis and the plasma accumulation of palmitate-enriched, linoleate-deficient triglyceride.


and:
on high fat diet B, there was less change in both fatty acids from baseline and a faster equilibration to concentrations that were similar to the concentrations in the diet and adipose tissue.

 

[papaya]

As I understand Dr. Peat, PUFAs are stored in cells rather than burned as fuel. So they can get dumped into the bloodstream as free fatty acids and create prostaglandins and participate in all sorts of inflammatory reactions.

But where is evidence of this? I have seen other evidence that satfat is stored and PUFAs burned first...

Any studies that back up Peat?

Thank you!

have you gotten a definitive answer to this yet? i've been so curious about this.