I've been reading through some papers on a gut-brain connection that regulates food intake and blood nutrient balance. I've learned some interesting things.
First of all, when fat hits your small intestine (especially long-chain fatty acids), it sends a message to the brainstem via the vagus nerve. This rapidly inhibits eating behavior.
The hypothalamus can also inhibit glucose production by the liver in response to fat in the bloodstream, by sending it signals via the vagus nerve.
A recent paper that got me interested in all this showed that when you put fatty acids on the upper small intestine, it sends a signal to the brain, which then sends a signal to the liver, increasing insulin sensitivity and decreasing glucose production.
The upper small intestine is not just a passive nutrient sponge. It's a very active player in the body's response to food, coordinating changes in food intake and nutrient disposal.
Interesting post. I'm curious, is it clear why the fat receptor cells become less sensitized after a few days of a high fat diet?
A total guess, but from an evolutionary standpoint, maybe it makes sense higher fat eating days would come and go in waves -- a few days here when a fatty animal is hunted, and then a few days without a lot of fat until another?
I don't know, I was busy picking berries apparently. Which isn't too different from how I turned out.
I don't know why. Remember this data is in mice, who don't go hunting for fatty game.
I suspect the desensitization mechanism is absent or irrelevant in humans. At least those with variable energy intakes.
I guess those papers you cited are further confirmation that LF diets aren't the most effective strategy to counter obesity.
So if one were to take some "fat pills" (for example some fish oils, or concentrated omega-3/6 pills) 15 to 30 minutes before dinner, one may be able to leave the table more satisfied on less food?
I wouldn't be comfortable making that prediction, I think it would have to be tested empirically. I'm also not confident that the system works the same in mice and humans, since mice don't seem to be as well adapted to a high-fat diet as humans.
If direct administration of lipids into the upper intestine suppressed glucose production, could this be somehow useful in cancer therapies targeting the reduction of gluconeogenesis?
Perhaps. It would depend on whether the gut becomes desensitized to the signal (as in mice) or not.
Maybe (as with much other dietary "research") they're looking at it back-asswards.
Maybe the fat returns insulin sensitivity to "normal" from which it has been altered by the excess carbs which are normal in the modern diet and especially in the research diets?
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