The Pennyslvania State University study, published in the August issue of the Journal of Nutrition, observed the effects of the 'stop eating' hormone cholecystokinin (CCK) on two groups of rats.
Over a 20-day period, one group was fed a long-term high-fat diet, and the other a long-term low-fat diet with an equivalent calorie loads. For three hours a day, both groups were given access to a high-calorie, high-fat snack, that rats find delicious.
When they administered CCK to the rats, the researchers noticed that those on the low-fat diet reigned in their consumption of the snack food but those on the high-fat diet continued to eat as much as 40 percent more.
"These results suggest that a long-term, high-fat diet may actually promote short-term over-consumption of highly palatable foods high in dietary fat by reducing sensitivity to at least one important feedback signal which would ordinarily limit eating," said lead author Dr Mihai Covasa.
CCK is released in the small intestine in the presence of fat or protein, triggering the activation of nerves to send 'stop eating' signals to the brain.
No human study has been carried out into the relation between CCK and snacking, but the authors draw attention to studies where human subjects have reported increased hunger, declining fullness and a desire to eat more when on a high fat diet. These subjects were found to have more CCK in their bloodstream but were less responsive to it.
Interestingly, despite gorging on the snack food the high-fat diet rats were no fatter than those on the low fat diet. This is because, unlike humans, rats have an innate ability to compensate for over consumption. The high-fat group simply adjusted their routine food consumption to compensate.