Tucker posted an excellent discussion of this paper on his blog. Go read it:
Fat Quality Influences the Obesogenic Effect of High Fat Diets
The basic conclusion is that feeding rats a high fat diet makes them fat. If it is PUFA based, including a generous amount of omega 3 alpha linolenic acid, it will cook their liver (figuratively speaking... in actuallity it converts their liver to being full of peroxidised PUFA, en-route to cirrhosis). I have an anecdote-type post on the problems of being married to a cardiologist if you happen to be alcohol addicted somewhere. I really ought to dig it out and hit post.
So. The problems with the paper:
The rats on the PUFA diet, with the gross fatty livers, were less obese than the lard fed rats, had better lean body mass percentage and much better brown adipose tissue hypertrophy and fat oxidation.
The bottom line: If you want look slim and well muscled in your coffin then a safflower oil diet with a heavy dash of varnish might be a good choice...
The paper was not looking at insulin levels or insulin signalling so it doesn't provide the data we need to come to any conclusions but it has resonances to the comment Zoran made on the previous post.
The Protons Credo (believe if you so wish!) for the situation:
PUFA, of a carbon chain length which targets them for mitochondrial oxidation, input less FADH2 at mitochondrial electron transporting flavoprotein dehydrogenase (mtETFdh) than do saturated fats or MUFA. This lack of FADH2 input limits the ability to reduce the CoQ couple and facilitates electron flow down the electron transport chain (ETC) and so limits the generation of reverse electron transport through complex I. This damped RET limits the ROS generation (superoxide and H2O2) necessary to initiate insulin signalling under fasting and to limit excessive insulin signalling in the fed state.
So on a whole body basis PUFA maintain insulin sensitivity. Insulin acts, rather well, under PUFA compared to under saturated fat, in the fed state. It works less well in the fasted state.
A fed, insulin sensitive animal will do two things of interest on a medium carbohydrate, generous fat diet. It will utilise glucose easily in muscles to burn calories and it will continue to use glucose in adipocytes to esterify FFAs with glycolysis-derived glycerol, to store fat.
So the Protons thread expects insulin sensitivity to cause fat accumulation because of maintained insulin sensitivity in adipocytes at high levels of insulin signalling. The cost of this insulin sensitivity is obesity.
PUFA = obesity, soybean oil is the best, they used safflower here.
Slight aside: The insulin resistance associated with obesity is nothing to do with insulin per se. It is triggered by the fact that very large adipocytes leak free fatty acids irrespective of insulin levels. At elevated FFA levels more insulin is needed to translocate GLUT4s than at low FFA levels.
Back to the rats.
The lard fed rats are the most obese. The PUFA fed rats the least obese.
The lard fed rats are on about 10% of their calories as PUFA in their diet. They are probably almost as fat as a 10% PUFA diet would like them to be, ie their adipocytes are almost as distended as a 10% PUFA diet dictates. The rats are almost as fat as they need to be. They are doing this on 380kJ per day. Because the rats are only allowed a total of 380kJ of energy per day. Did you pick that up in the methods?
The PUFA fed rats want to be truely, grossly obese, much more so than the lard fed rats do, because they are on somewhere between 50% and 60% of their energy intake as PUFA. But there, in the hopper, is that same old 380kJ per rat per day. It doesn't matter how much your adipocytes are crying out for more fat, how empty they feel, how hungry they tell your brain to feel. There, in the hopper, is 380kJ.
These rats are intensely insulin sensitive because their adipocytes are "empty" compared to how thery would like to be. They are "starving" compared to how they would like to be. Their muscles respond to insulin's anabolic effect and I'd be willing to bet their growth hormone levels are through the roof and IGF-1 through the floor (another post there, GH, IGF-1 and starvation). Insulin is going to be low because any glucose released from the liver is easily utilised in the fed state. In the fasting state insulin fails to act effectively so that, while FFAs may be the same as in the lard fed rats, we know (from Figure 2) that lipids are being oxidised much more rapidly on a 24h basis.
PUFA sensitise adipocytes to insulin. Given the choice the animal will eat until obese and become insulin resistant due to adipocyte distension. Combine PUFA with starvation and insulin sensitivity will be maintained. Or enhanced.
Just the Protons view. Any other explanations welcome.
Of course people should ask how the action of PUFA compares to the action of metformin. They are superficially similar. That might need more doodles I'm afraid!