This paper is a gem.
Reducing the Dietary Omega-6:Omega-3 Utilizing α-Linolenic Acid; Not a Sufficient Therapy for Attenuating High-Fat-Diet-Induced Obesity Development Nor Related Detrimental Metabolic and Adipose Tissue Inflammatory Outcomes
What did they do? They fed rats chow or they fed them on one of four other diets enriched in PUFA. The extra PUFA were based around various mixtures of linoleic acid with alpha-linolenic acid, some were mostly corn oil, some were slanted towards varnish (flax/linseed oil). Total 18-C PUFA made up 9.4% of calories, ie was obesogenic, and this was identical for all of the high fat diets. Overall macros were identical in all of the high fat diets too. There was no sucrose. The rats were fed ad lib.
Here is the link to Table 1 which lists the compositions, it's too big for putting it up as a jpeg. Just look at how utterly fair the composition of the high fat diets were. Even if the absolute amount of linoleic acid in the lard is not accurate, there will be a consistent error across the diets and the results stay plausible. My only complaint is that there was no group where the omega-3 lipids predominated in the diet PUFA, a 50:50 mix was the maximum. Whereas the maximum omega-6 fed group got essentially all of their PUFA from omega-6 PUFA.
The second excellent feature is that the rats were neither semi-starved nor forcibly overfed. Rats are not people. They cannot be verbally asked to overeat to maintain a stable bodyweight nor to calorie restrict to lose weight. They will simply eat until they are no longer feeling hungry. If that happens while they are svelte or not until they are morbidly obese, the rats don't care.
Almost nothing. The chow fed rats, with around 3.5% of calories as PUFA, stayed at a reasonable weight. The obesogenic high fat diets (ie nearly 10% of total calories as PUFA) each caused almost exactly the same progression of obesity:
Can you see that the open squares group gain weight slightly more slowly than the other PUFA diet groups? This shows between week six and week 17. The two hashtags mark out a couple of time points where this achieved statistical significance. This slightly less obese group of rats is the group which ate the least alpha-linolenic acid, the most linoleic acid. This suggests that omega-6 PUFA are less fattening than omega-3 PUFA. I like that. Protons likes that.
The effect was fairly small and only shows as an early facilitation of weight gain. By the end of the study the rats and their adipocytes were all about as fat as they were going to get on 9.4% of calories from any family of PUFA.
You can easily hide this effect by under feeding (pair feeding to the same calories as a chow fed group or arbitrarily reducing overall caloric availability) or overfeeding (paid humans or intragastric cannula over-fed rats). If you are an omega-3 lover this can be necessary. But, given a decent study, it shows.
Consuming the 18-C omega-3 rich linseed oil/flax oil/varnish may not make you terribly much fatter than corn oil will eventually make you, but it should get you there quicker. The situation for EPA and DHA is different. Oxidising these will increase the cytoplasmic NADH:NAD+ ratio via peroxisomal oxidation (bad) and give reasonable mitochondrial function from oxidising the residual saturated caprylic acid C-8 (good), which is the normal fate of very long chain fatty acids of any ilk.
Executive summary: Omega-3 18-C fatty acids are more obesogenic than omega-6 18-C fatty acids. The effect is small but real, it might show better if all of the PUFA were alpha-linolenic acid rather than to 50:50 mixture used. It still makes me happy.
The Protons view (skip this if you're fed up with hearing it over and over again)...
I consider that the mitochondrial oxidation of PUFA will always show as increased peak insulin sensitivity. The cost of that increased insulin sensitivity is fat gain. The fat gain eventually eliminates any benefit from the initial increase in insulin sensitivity. Forced manipulations of the food intake downwards will preserve the intrinsic insulin sensitivity at the cost of chronic hunger. So when high PUFA-fed lab-rats are "pair fed with the chow group" the PUFA rats will look really good, metabolically. The converse, encouragement to overeat, based on avoiding "accidental" weight loss (weight loss is a huge confounder in studies of hepatic lipid accumulation from almost any intervention, PUFA included) by weekly weighing to maintain weight will mask any benefits from saturated fat induced adipocyte insulin resistance. Stacking the deck is crucial to the result you want to get.