I think we have to start with the results section of Cao et al's very interesting (and free to study if you want all the detail) paper:
Identification of a Lipokine, a Lipid Hormone Linking Adipose Tissue to Systemic Metabolism
As always, the paper is a superb piece of detective work featuring a superabundance of genetically engineered mice from the C57BL/6J background fed an high fat diet, the nature of which doesn't make it in to the methods, but we can just assume that it's all the usual fare. They started from the protective effect of knocking out certain fatty acid receptors in the mice, which prevented the development of metabolic syndrome, and ran with this concept for the massive project detailed in the paper. It's big. It ended up with them doing the following to confirm that they got it correct. From the very end of the results:
"To define the effects of individual fatty acids on metabolic regulation, we prepared Intralipid with triglycerides composed of a single fatty acid, either TG-palmitoleate or TG-palmitate. Infusion of either lipid resulted in a two-fold increase in total plasma FFA levels with similar dynamics (Figure S13). While TG-palmitate suppressed the entire proximal insulin-signaling pathway including activation of insulin receptor and phosphorylation of insulin receptor substrate 1, 2 and AKT in liver, TG-palmitoleate strongly potentiated these insulin actions (Figure 7A). We observed similar effects of both lipids on muscle tissue where palmitoleate enhanced and palmitate impaired insulin signaling (Figure 7B)."
It's a switch, at the crude level of Intralipid infusions. Viewed macroscopically:
Palmitoleate = insulin sensitive
Palmitate = insulin resistant
I may have mentioned this before!
If you take a light switch apart, under the plastic there are some metal parts. The metal provides a sea of probability through which electrons can flow, provided the metal is continuous from light bulb to the powerstation (pax transformers). Or not flow, if we replace a few mm of metal with a few mm of room air.
If we accept that superoxide from complex I reverse electron transport is insulin resistance, then fatty acid binding proteins are a macroscopic overlay over this process, they are part of the plastic of the switch.
Superoxide never leaves the mitochondria, it probably converts to H2O2 to talk to the nucleus or acts locally to activate transcription factors which then talk to the nucleus. Adipocytes don't talk to muscles using superoxide either. The intermediary they use appears to be palmitoleate, probably the ratio of palmitoleate to palmitic acids, once you get away from bulk Intralipid infusions.
Why is it arranged this way? The body has to know what substrates are available. Ignoring protein, carbohydrate talks to the body through insulin, and through insulin transporting glucose in to adipocytes. That's the next post.
There: Not a mention of FADH2 or NADH. Even if I'm thinking about them, as per the last post...
BTW, Charles commented on the depressing amount of superoxide associated with a high fat, low carb diet. True, but about as scary as going for a walk at the brisk-but-not-excessive pace which is reputed to burn fat best. Burning fat is what LCHF eating is all about. Useful if you don't have the hours a day to walk for health purposes. Walking seems to be quite good for you!