Does Coconut Oil stimulate appetite?

A comment I read on PaleoHacks led me to this article on Livestrong:  Does Coconut Oil increase your appetite?  It cites the following study: Ingested Medium-Chain Fatty Acids Are Directly Utilized for the Acyl Modification of Ghrelin .

ABSTRACT:

Ghrelin, an acylated brain and gut peptide, is primarily produced by endocrine cells of the gastric mucosa for secretion into the circulation. The major active form of ghrelin is a 28-amino-acid peptide containing an n-octanoyl modification at serine that is essential for activity. Studies have identified multiple physiological functions for ghrelin, including GH release, appetite stimulation, and metabolic fuel preference. Until now, there has not been any report detailing the mechanism of ghrelin acyl modification. Here we report that ingestion of either medium-chain fatty acids (MCFAs) or medium-chain triacylglycerols (MCTs) increased the stomach concentrations of acylated ghrelin without changing the total (acyl- and des-acyl-) ghrelin amounts.

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High Protein Diet Induces Sustained Reduction in Ad Libitum Intake Despite Diurnal Leptin Compensation

I've written several hundred posts on this blog.  There are some, especially from early on in 2010, that I would really like my readers to see, and I sure don't expect folks who are just finding this blog now to go back and read everything to find some that I feel are key.  I refer to this study quite often because I think for those finding themselves gaining a little bit each year and not wanting to hop on some "diet rollercoaster", there is merit to -- especially for us women -- upping the protein as a percentage in the diet.  So when I was compiling graphics for the 24 Hour Leptin Profiles post, this study was the first I knew to go to for a graphic.  So, I'm bumping the original, adding a little emphasis to the text but not changing it, and I'll add some commentary on leptin at the end.  

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Original Publish Date:  4/30/10

A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations

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Hyperinsulinemia and Anorexia?

In the course of a discussion over at Jimmy Moore's forum I came across something I did not know.  Anorexics -- the thinnest among us! -- can also become hyperinsulinemic!!!!   How can that be??  

If it's all about the insulin causing fat accumulation, one would think this condition would result in any dietary intake getting trapped in the fat tissues, making it unavailable to the anorexic for fat-burning, resulting in voracious hunger.  

But we would expect the anorexic to have very low postprandially-induced insulin levels.  No matter what they eat, they don't eat much.  So, where is this insulin coming from?  

It would seem to be, yet again, a defense mechanism of our bodies.  I've come across quite a bit of contradictory observations on this.

For example, in this article, anorexics had lower postprandial insulin responses and higher metabolic rates of insulin clearance and describe anorexia as being associated with improved insulin sensitivity.  They also have decreased basal insulin levels.  The authors propose this is an adaptive mechanism to protect the anorexic from hypoglycemia.  Here is another article describing improved insulin sensitivity in anorexia.  The hormonal levels from that study are shown below.

However searching on hyperinsulinemia and anorexia yields some interesting hits:

Hyperinsulinemia; a mediator of decreased food intake and weight loss in anorexia nervosa and major depression.

A brief review is made of the role of insulin in satiety and in the control of body weight, and of the newly available techniques to accurately quantify secretion, hepatic extraction, and post-hepatic delivery rates of insulin. Neural, metabolic, and endocrine stimuli affect insulin secretion. The hypothesis is therefore compatible with several etiologic factors leading to hyperinsulinemia in anorexia nervosa and major depression, and resulting in decreased food intake and weight loss.

There's also this case study (can't find anything of this paper)

How does the hyperinsulinemia develop?  Usually it's from insulin resistance, and IR would seem to be a reasonable physiological adaptation to starvation -- so as to preserve glucose for the tissues that need it most.    Elevated cortisol that is associated with anorexia could be the cause.  Perhaps the changes in insulin sensitivity are time/progression dependent, with one occurring early on, the other developing later?

Still, it is interesting that the elevated insulin is associated with further REDUCED intake, not vice versa.