Regular readers may recall a previous post on the discovery that we have specific oral sensory receptors that allow us to sense the ‘fattiness’ of food – a function that makes a lot of sense, given that dietary fat provides the densest source of caloric intake.
Now, Nicholas DiPatrizio and colleagues from the University of California, Irvine, have discovered that these oral dietary fat sensors activate a powerful ‘addiction-type’ mechanism in your gut that serves to promote further fat intake – their study is published in a recent issue of the Proceedings of the US National Academy of Science.
For their studies, the researchers used a well established ‘sham feeding’ model in the rat, where liquid diets eaten by the animal can be drained from the stomach via a chronically implanted gastric cannula, thereby preventing them from reaching the small intestines.
Using this model, the researchers showed that ‘sham feeding’ of a high-fat diet resulted in the potent activation of endocannabinoids in the early part of the small intestine by altering enzymatic activities that control endocannabinoid metabolism. The endocannbinoids (cannabis-like compounds produced in the body) are well known to play an important role in regulating ‘rewarding’ feeding behaviours.
This effect was abolished by surgical transection of the vagus nerve showing that the stimulation of these changes in the gut is driven through a centrally mediated neuronal pathway.
Furthermore, the local application of cannabinoid type 1 receptors blockers (e.g. rimonabant) in the small gut, reduced increased sham fat ingestion.
In other words, this study shows that oral sensing of fat sends a signal to the brain, which in turn sends a signal to the gut leading to formation of endocannabinoids, which in turn re-enforce fat eating.
This is probably why, just eating one piece of fatty food (say one potatoe chip or French fry) is so hard – simply eating one makes you want to continue eating till the whole bag or plate is empty.
Unfortunately, the drug rimonabant, used to effectively block this effect in this study, is no longer available for obesity management (it was withdrawn due to its negative impact on mood), but it may well be that other CB-1 inhibitors that do not enter the brain may prove to be effective to reduce fat intake.
Or, in the words of the authors:
“Our findings identify the gut endocannabinoid system as a critical component of the positive feedback mechanism that drives fat intake and suggest that therapeutic strategies aimed at restraining small intestinal endocannabinoid activity might help to selectively reduce the overeating of fatty foods.”
In the meantime using strategies based on limiting portion size, e.g. asking for a small serving of fries or transferring a small portion of chips into a separate bowl, while leaving the full bag in the pantry, may be the best strategy to thwart this mechanism.
Dipatrizio NV, Astarita G, Schwartz G, Li X, & Piomelli D (2011). Endocannabinoid signal in the gut controls dietary fat intake. Proceedings of the National Academy of Sciences of the United States of America PMID: 21730161