These matter for me because rodents (other than the C57Bl/6 mouse) mostly have perfectly normal mitochondria and so provide a reasonable model for extrapolation to humans.
I cannot explain these via the F:N ratio of the lipids so they then challenge my whole hypothesis. I guess the first possibility is that I am simply incorrect so should abandon my pet ideas. Possible, but not easy.
Second is that the medium chain triglycerides in coconut oil (and butter?) are handled differently from longer chain lipids. They certainly are, with limited penetration in to chylomicrons and marked diversion to the liver via the portal vein as free fatty acids. The liver "sees" them, adipocytes don't. To some degree, nothing in biology is 100%.
Also the fate of medium chain fatty acids in peripheral cells, when they do get there, may be different to longer chain fatty acids. I am reminded of the very poor insulin secretagogue effect of octanoate on the isolated pancreatic preparation in
The Insulinotropic Potency of Fatty Acids Is Influenced Profoundly by Their Chain Length and Degree of Saturation
The Insulinotropic Potency of Fatty Acids Is Influenced Profoundly by Their Chain Length and Degree of Saturation
which makes octanoate look worse than linoleic acid in promoting insulin secretion (and presumably the same applies to generating insulin resistance in target cells). This would fit with medium chain fatty acids being obesogenic despite their desirable F:N ratio, but without any insight as to how or why.
The final possibility is that the effect of linoleate oxidation differentially affects high and low fat diets. Under low fat diets the ability to resist insulin comes, in my opinion, from the input of electrons via the glycerophosphate shuttle converting an NADH input to an FADH2 input to the electron transport chain. From fatty acids it's all about NADH vs FADH2 at electron transporting flavoprotein dehydrogenase. Do these mechanisms kick in at identical levels of caloric ingress or are there subtleties of high vs low fat diets?
So lots of pondering and no answers.
I have extracted a little more information from this paper
The group didn't measure the linoleic acid content of the diets they fed but their intervention diets were composed of materials with very tightly defined LA contents, so their calculated amounts are likely to be accurate.
Here we have the growth rates of mice on chow (5001 "vivarium" rodent food termed Viv) or on an high fat diet based on fully hydrogenated coconut oil + 2% of calories LA or partial replacement of coconut oil to give 10% of calories from LA. Here are the growth curves:
The impression here is that the blue line of the fully hydrogenated coconut oil diet (+2% LA) is more fattening than the (grey line) Vivarium chow, though not as badly as the orange line of the 10% LA diet.
You could start to think about all of the differences between 5001 and the various high fat diets but the simplest is to extract the LA contents from Table 1:
which lets us label the growth graphs with the LA contents thus:
An interesting question might be where 4% LA (Surwit-like) diet might have placed the growth curve, even more interesting would be to almost half the LA% to the 1.2% supplied by 5001.
That's not something that is easy to find. Obviously there is a certain amount of work with linoleic acid free diets used to show the problems and benefits of essential fatty acid deficiency in rodents, usually based around fully hydrogenated coconut oil. I quite like this one where borderline essential fatty acid deficiency is remarkably protective against systemic lupus in a mouse model using non-hydrogenated coconut oil
So limiting linoleic acid to levels present in non hydrogenated coconut oil (less than 1% LA) allows growth and health in this model while producing zero obesity using approx 40% of calories from coconut fat.
So it appears that the obesogenic effect of coconut oil based diets is not intrinsic to the MCT content but some obesogenic effect of linoleic acid on this background is present at 2% of caloric intake and spectacularly so at 10% of calories.
Here's a little histopathology for those PUFA-philes who follow any of the conventional diet gurus on 'tinternet. If you like soybean oil as a health food, you go for it, fine by me!
Liver histopath after 35 weeks on 5001 chow. Red dots are lipid:
On fully hydrogenated coconut oil with a mildly obesogenic 2% of calories as soybean oil derived linoleic acid:
and on a cardiological nirvana of 10% calories from soybean oil derived linoleic acid:
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Clear balloon cells are very poorly liver cells. Now, I wouldn't wish such a liver architecture on to anyone but if I was pushed in to a corner I might consider Prof Risérus, lead author of
as being a possibly deserving recipient.
Co-authors Walter Willett and Frank Hu might be candidates too.
Peter
