I guess beef or other herbivorous meat, or any lean meat plus butter might be worth a shot.
My simple monkey brain got--a FADH reaction that's not as present when oxidizing polyunsaturated fat as with saturated fat generates extra electrons (or an extra pathway for electron generation). More electrons equals more potential energy production--more electrons also makes for higher production of superoxide, the proposed molecular signal for insulin resistance.
I wonder about other factors--rate of ATP production, more direct signalling effects of various fatty acids. Whether there are citric acid cycle metabolite consequences of changing fadh/nadh ratios, whether there's a difference in malonyl-CoA production--malonyl CoA is molecular switch for fatty acid/triglyceride synthesis, generally when these are increased, fatty acid oxidation is decreased, so it's also a switch to some degree for fat versus carb oxidation (high metabolism of glucose increases malonyl-CoA, that makes sense, increased fat synthesis as an excess glucose sink).
There's also a series of studies in mice that proposes a different mechanism for a fattening omega 6 effect--at 8 percent linoleic acid, a high, low or moderate fat diet are all fattening, bring it down to 1 or 2 percent, it's not. The omega 6 is used to produce endocannabinoids, blocking their production reverses the fattening effect. Maybe not that surprisingly in humans blocking endocannabinoids has a risk for depression.
One area that seems relevant and also supports to some degree the palmitic acid/insulin resistance hypothesis--single-cell studies looking at lipotoxicity. Cells bathed in palmitic acid and glucose (but not palmitic acid or glucose) produce an excess of lipid byproducts. One is ceramide, there's a lot of study on it as causing insulin resistance and cellular damage. Adding some oleic acid is protective (at least in some studies), the proposed mechanism is that triglyceride synthesis, which increases with the addition of the oleic acid to the medium, gives a safer pathway for disposal of the excess free fatty acids, the production of ceramide is decreased. It might not be so much the decrease in free fatty acids but the fact that when the triglyceride pathway increases, the pathway to ceramide synthesis tends to be sort of shut down. This "protective" effect of oleic acid does come with increased triglyceride storage in the cell versus just palmitic acid being present. I've seen this in liver and beta cell studies.
There are also some studies on polyunsaturated fats having an effect through Peroxisome proliferator-activated receptors of encouraging fatty acid oxidation (among other things, none of which I can currently name
), maybe this makes sense as something needed to ameliorate what might otherwise be a more fattening effect?