Insulin mimesis without NOX enzymes (5) MCT plus linoleic acid

You can become obese by having your adipocytes fail to limit insulin signalling. That is what linoleic acid plus an insulogenic diet does, pure Protons.

You can also become obese by making your liver alone insulin resistant in combination with an insulogenic diet. The Surwit diet approach.

These concepts put us in to a position where we can examine this study, HT to Tucker:

Ability of high fat diet to induce liver pathology correlates with the level of linoleic acid and Vitamin E in the diet

In particular we can look at these curves:

Obviously blue circles are the chow and red triangles show the 8% linoleic acid, high overall fat diet. The latter is as obesogenic as you might expect. The surprising curve is the beige 1% LA line. This diet is clearly less obesogenic than the high LA diet but is not exactly slimming when compared to the chow line. And it supplies only 1% of calories from LA.

So do *all* high fat diets make you (and rodents) obese?

The macro of the diets are described in Table 1. I've cut off the vitamin E parts as they are a different subject altogether and might be worth a post some day.

If you come at this from the point of view that saturated fats are slimming and LA is obesogenic then the low LA diet causing a significant level of obesity is a paradox.

In the legend to Table 1 there is a link to supplementary information which I followed, trying to find whether fructose was included in the diets (the paper doesn't actually say) but I did find out that the bulk of the fat in both the 35% fat diets is, as you may have guessed, fully hydrogenated coconut oil.

The 1% low LA diet is a classical Surwit derivative (possibly without the sucrose, I don't think it matters) and is inducing hepatic insulin resistance via ETC derived high levels of ROS to allow penetration of glucose/insulin to peripheral sites. The adipocytes see too much insulin for too much time and get fat.

The 8% high LA diet has exactly the same problem from its MCT components as the 1% LA diet but this time it's compounded by peripheral adipocyte exposure to high levels of LA causing pathological insulin sensitivity, delivered directly via chylomicrons from the gut, bypassing the liver. They get high insulin exposure secondary to MCTs acting in the liver to allow increased glucose/insulin to the systemic circulation PLUS a pathological inability to resist insulin's fattening signal in the periphery via LA, ie adipocyte Protons effect on top of localised hepatic insulin resistance. Double wammy, double weight gain.

Peter