Dr. Mihai Covasa, assistant professor of nutritional sciences and a member of the Penn State Neuroscience Institute, led the study. He says, "When we gave the rats doses of a 'stop eating' hormone, the rats on the low fat diet significantly suppressed their intake of the snack but not the rats on the high fat diet."

Covasa adds, "These results suggest that a long-term, high-fat diet may actually promote short-term overconsumption of highly palatable foods high in dietary fat by reducing sensitivity to at least one important feedback signal which would ordinarily limit eating."

The results are detailed in the current (August) issue of the Journal of Nutrition in a paper, Adaptation to a High-Fat Diet Leads to Hyperphagia and Diminished Sensitivity to Cholecystokinin in Rats. The authors are David M. Savastano, who recently earned his master's degree under Covasa's direction, and Covasa.

The 'stop eating' hormone used in the study was cholecystokinin or CCK. CCK is released by cells in the small intestine when fat or protein is present. The hormone's release activates nerves that connect the intestine with the brain where the decision to stop eating is made.

Previous studies with human subjects showed that those on a high fat diet have more CCK in their bloodstream but are less responsive to it. They typically report feeling increased hunger and declining fullness and eat more.

No human study of snacking and CCK has been reported. This study, with rats, is the first to link diminished sensitivity to CCK following exposure to a high fat diet and overconsumption of a high calorie, high fat snack.

In the current study, the rats were only given access to the high calorie, high fat snack for three hours a day. The rest o
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Contact: Barbara Hale
bah@psu.edu
814-865-9481
Penn State
2-Aug-2005