cAMP-dependent signaling regulates the adipogenic effect of n-6 polyunsaturated fatty acids.
This study was set out to simply help resolve the conflicting information coming from various studies about whether omega6 are pro-adipogenic or not. Linoleic acid is a precursor of arachidonic acid, and it is arachidonic acid that is more the focus of this study.
To cut a long story short, the researchers found that keeping carbohydrates low in the diet was able to turn omega6 from fattening into ( potentially ) slimming. Mice fed a higher protein lower carb diet, high in PUFA remained quite slim, while the higher carb fed mice became obese.
The way this works is, by keeping carbs low, the glucagon/insulin ratio of the diet is elevated , leading to increased cAMP in adipose tissue ( glucagon elevates cAMP in adipose tissue ). This increased cAMP drives the production of arachidonic acid towards the prostaglandin F2α, which has been shown to have strong anti-adipogenic functioning.
Below is the important graph in the study imo....
As you can see, prostaglandin F2α is significantly higher on the low carb, higher protein diet.
The diets fed to the rodents are below...
The starch component is 9.486, not 9 thousand. Dont be confused like I was...
Anyway, some of you may notice that the change was in the sucrose, going from 9% sucrose to 43% sucrose may probably make you obese regardless of the other stuff in the diet......*shrug*
The feed efficiency was strikingly different between the mice, to quote..
In the high protein group, 467.8 kcal were needed to produce a weight gain of 1 g, whereas the high carbohydrate group only needed 67.8 kcal to produce the same weight gain, which almost exclusively represented an increase in adipose tissues.
In still yet another study, researchers were able to show that knockout of the enzyme Akr1b7 which produces prostaglandin F2α, automatically produces obesity ( they noted both hypertrophy and hyperplasia in this model ) . In particular they found increased expression of the lipogenic gene's, fatty acid synthase and scd1 in the adipose tissue of the knockout group.
Interestingly, in the second study using high-fat-diet, the knockout mice still managed significantly higher fat mass despite slightly reduced food intake.
Lastly, to expand on the function of fatty acid synthase in adipose tissue, another group of researchers have put forward the idea that the function of fatty acid synthase may not exactly be to make fats de novo for storage per se, but rather the function of fatty acid synthase may be to synthesize a ligand for PPARgamma.
It also looks like prostaglandin F2α helps inhibit PPARgamma.
So in conclusion I think, the fattening potential of omega6 PUFA should be considered in context. Anecdotally I noticed especially good weight loss when I combined very low carb with large servings of peanuts, 150g+ per day.