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Brain Pleasure Pathway Responds to Calorie-Rich Foods, Not Just Sugar Flavor


DURHAM, N.C. – Researchers at Duke University Medical Center have discovered that the brain can respond to the calorie content of food, even in the absence of taste.

Their findings about the brain’s dopamine-reward system may help shed light on why many people who drink diet sodas still gain weight. A mismatch between artificially sweet taste and zero calorie content may lead to some kind of rebound eating that may in part be explained by these results: the brain is wired to respond to both calorie content and sweetness.

For years, scientists have known that when mammals, including humans, taste sweet foods, dopamine levels increase in the ventral striatum, a brain region related to reward and reinforcement. The neural pathways have been well established for palatability (the power of a food to make one eat it spontaneously and with gusto) as food is being eaten. With this set of experiments, the Duke team studied the brain’s response to food after it was ingested.

Using mice that lacked sweet-taste receptors as a model, the researchers studied behavior as well as neural responses in the study published in the journal Neuron on March 27.

Mice that were unable to taste sweetness, either in real sugar (sucrose) or artificial sweeteners (sucralose), developed preferences for real sugar but not non-caloric sweetener. Mice with normal taste receptors also developed the same type of preferences.

“The fact that sweet-blind animals are conditioned by sucrose only, demonstrates that they can detect this sugar because of its caloric content and adequately modify their behavior to obtain this reward, independent of taste input,” said researcher Albino Oliveira-Maia, of the Duke Department of Neurobiology and the University of Porto in Portugal.

To reach this conclusion, the researchers first confirmed that one set of mice did not exhibit a taste motivated-preference for sucrose. Normal mice naturally preferred various concentrations of sugar solutions to water, but mice without functional sweet taste pathways did not show any preference.

The scientists then explored preference in mice that were both hungry and thirsty. During conditioning sessions with two bottles, both the normal mice and the taste-impaired mice consumed more sucrose than water. When conditioning was complete, preference tests with two bottles of water was conducted. Both groups of mice preferred the sipper that had been filled with sucrose during conditioning sessions.

Substituting an artificial sweetener, sucralose, for the sucrose solution, the scientists ran the conditioning experiment again and found that while the normal animals consumed much more of the sucralose solution than water, the sweet-blind mice consumed about the same amount of both. Neither group showed a preference for the sucralose sipper during the test session.

The conclusion: both groups of mice were conditioned by sucrose, which must have depended on the calories obtained from this solution.

The researchers also found significant differences in dopamine levels during eating, regardless of the ability to taste food. Normal mice showed a rise in dopamine when they gobbled the artificial sweetener solution, indicating palatability even without calories present. Mice without sweet taste released dopamine only during sucrose intake, even though they could not distinguish between the taste of water and sucrose. This confirmed that dopamine can be released in the ventral striatum by either sweet taste or caloric content.

It may mean that the role of dopamine transmission (the pleasure principle) in overeating and obesity might not be restricted to taste alone – dopamine signaling also can influence behavior by indicating a food’s caloric value.

The authors also demonstrated that neurons in the same area of the brain had significantly higher responses when taste-impaired mice were consuming sucrose in comparison to sucralose.

“This suggests that the calorie-dependent release of dopamine in the ventral striatum has an impact on the response properties of populations of neurons in the same area,” said Miguel Nicolelis, professor in the Duke Departments of Neurobiology and Biomedical Engineering and the Center for Neuroengineering. “Thus, the brain dopamine pathways might also perform an action we had not previously identified, by detecting gastrointestinal and metabolic signals.”

“The metabolic effect we see may also feed into the same neuronal pathway that we associate with pleasure,” said Marc Caron, professor in the Duke Department of Cell Biology.

Other researchers included Sidney Simon of the Duke Departments of Neurobiology and Anesthesiology and the Center for Neuroengineering; Ivan de Araujo of the Department of Neurobiology and the Center for Neuroengineering; and Tatyana Sotnikova and Raul Gainetdinov of the Department of Cell Biology.


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