A few more thoughts building on F:N ratios of differing metabolic substrates:
Each cycle of beta oxidation (assuming an even numbered carbon chain fully saturated fatty acid) produces one FADH2, one NADH and one acetyl-CoA. This gives a total of 2FADH2 inputs and 4 NADHs per cycle of beta oxidation. But the very last pair of carbon atoms in a saturated fat do not need to go through beta oxidation as they already comprise acetate attached to CoA, so they can simply enter the TCA as acetyl-CoA. This last step only produces 1 FADH2 and 3 NADHs, with no extras.
So the shorter the fatty acid, the less FADH2 per unit NADH it produces. Short chain fatty acids like C4 butyric acid have an F:N ratio of 0.43 while very long chain fatty acids, up at 26 carbons, have an F:N ratio of about 0.49.
As Dr Speijer points out, differing length fatty acids are dealt with differently. Very short chain fatty acids head straight for the liver and get metabolised by hepatic mitochondria immediately. Any excess acetyl-CoA gets off-loaded as ketones.
Very long chain fatty acids end up in peroxisomes for shortening, usually to C8, which is then shunted to mitochondria for routine beta oxidation. Of course peroxisomal beta oxidation generates zero FADH2, except that from acetyl-CoA, because peroxisomal FADH2 is reacted directly with oxygen to give H2O2. And heat, of course.
Bear in mind that the ratio of F:N generated by a metabolic fuel sets the ability to generate reverse electron flow through complex I and subsequent superoxide production, macroscopically described as insulin resistance.
So fatty acids up to C8 are cool, dump them to the liver and make a few ketones. Very long chain fatty acids over C18, shorten to C8 in peroxisomes, shift them to mitochondria and make some ketones if needs must. The F:N ratio of C8 is about 0.47, a value chosen by metabolism as the end product of peroxisomal shortening. The number is important. Actually the number is even lower as peroxisomal beta oxidation generates the NADHs of beta oxidation, just not the FADH2s, but why allow facts like this to spoil a great argument. C8 from breast milk and/or coconuts seems fine and has that F:N ratio of 0.47.
Now the area of interest is, of course, C16, palmitic acid. This has an F:N ratio of about 0.48, almost as superoxide generating as a C26 fatty acid up at 0.49. And palmitic acid does, without any shadow of a doubt, produce macroscopic insulin resistance. That's 15 FADH2s and 31 NADHs.
So an F:N of 0.47 is not a serious generator of superoxide and an F:N of 0.48 is.
What happens when we drop a double bond in to palmitic acid? Mitochondrial beta oxidation generates FADH2 as it drops a double bond in to the saturated fat chain. If the double bond is already there, hey, no FADH2!
Palmitoleate has one double bond. This of course gives 14 FADH2s and 31 NADHs, an F:N ratio of 0.45.
C8 caprylic 0.47, chosen by peroxisomes to hand to mitochondria
Adding a single double bond to palmitic acid drops its F:N ratio from significantly superoxide generating to minimally superoxide generating. It looks like a switch to me.
I just love the way the numbers pan out. Of course we can now go on to what these number signify and what determines unsaturation. And uncoupling too, I guess. We are then back to insulin and stearoyl-CoA desaturase and also de novo lipogenesis. It might be worth an aside to PUFA and how these behave too, especially in adipocytes.