Binge Eating: What Happens to the Brain When Pleasure Disappears?
- Lidi Garcia
- Apr 7
- 4 min read
Eating too much fat can make the brain work differently, decreasing the feeling of pleasure when eating. In tests on mice, scientists saw that a fatty diet made the animals lose interest in tasty foods, even when they were easy to reach. This happened because parts of the brain that control pleasure were "disconnected". They also discovered that a substance called neurotensin is linked to this, and that, by correcting its levels, it is possible to reverse the problem. This study helps to better understand how obesity affects the brain and may pave the way for new treatments for eating problems.
Our brain has a system that controls the desire and pleasure of eating, called the mesolimbic dopaminergic system. It includes a group of dopaminergic neurons, located in a region of the brain called the ventral tegmental area (VTA).
These neurons send signals to another area in the nucleus accumbens (NAc), which helps regulate motivation and pleasure associated with food. When we anticipate or eat something tasty, these neurons fire signals, encouraging eating behavior.
However, research shows that eating high-fat foods for a long time can decrease this activity in the brain, in both mice and humans. This means that the brain’s reward system can become “dysregulated,” reducing the motivation to seek out pleasurable foods, which can influence weight gain and obesity.
In addition to dopamine, the nucleus accumbens also has inhibitory neurons that communicate with the ventral tegmental area using a substance called GABA. These neurons influence feeding behavior, but their role is not yet fully understood.
Previous studies suggest that stimulating this connection between the nucleus accumbens and ventral tegmental area can increase reward behaviors, such as the pursuit of tasty food.
To better understand how obesity affects this mechanism, scientists fed mice a high-fat diet for a long period of time (called a High Fat Diet), analyzing their feeding behavior and the brain signals involved in this process.
The researchers used mice of the C57Bl/6 strain and divided them into two groups:
Control group: Fed a standard diet.
HFD group: Received a high-fat diet for a long period of time.
The goal was to simulate the effects of excessive consumption of high-calorie foods, such as fast food, on the animals' brains and behavior. The scientists analyzed how the mice reacted to the food in different ways.
Food preference in the cage: Both groups were given access to regular chow and a high-fat chow, to see which they preferred. As expected, the mice in the High Fat Diet group consistently chose the fattier chow.
Hedonic feeding test: The mice were placed in a new environment where high-calorie foods were offered without any effort required to obtain them. Surprisingly, the mice on the high-fat diet showed less interest in these foods, suggesting that their brains no longer found them as pleasurable.
To understand what was happening in the brain during these behaviors, the scientists recorded the activity of neurons in real time. They focused on two main regions:
Nucleus Accumbens (NAc) – which regulates the pleasure associated with food.
Ventral Tegmental Area (VTA) – which contains dopamine-producing neurons responsible for stimulating the motivation to seek out tasty foods.
Using advanced techniques, the scientists measured how neurons in these areas activated when the mice were given pleasurable food. In the mice on a regular diet, neural activity in the Nucleus Accumbens and Ventral Tegmental Area was synchronized with hedonic eating behavior.
In the High Fat Diet mice, however, this relationship was lost, suggesting that obesity alters the way the brain processes the pleasure of eating.
To test whether it was possible to restore the motivation to eat pleasurable foods, the scientists used optogenetics, a technique that allows specific neurons to be activated or inactivated using light. They implanted optical fibers into the mice's brains and artificially stimulated the pathway between the Nucleus Accumbens and the Ventral Tegmental Area.
Optogenetic Technique
In mice on a normal diet, this stimulation increased the desire for pleasurable foods. However, in High Fat Diet mice, the stimulation had no effect. This reinforces the idea that chronic fat consumption profoundly alters this brain circuit.
The researchers then investigated whether a chemical called neurotensin could be involved in the loss of food motivation observed in the High Fat Diet mice.
They found that the High Fat Diet mice had reduced levels of neurotensin in the pathway between the Nucleus Accumbens and the Ventral Tegmental Area. When they blocked the action of neurotensin in healthy mice, these animals also lost the pleasure of eating high-calorie foods.
On the other hand, when they artificially increased neurotensin levels in the High Fat Diet mice, the desire for palatable foods was restored.
The results showed that excessive fat consumption alters the functioning of brain circuits that regulate food pleasure, making high-calorie foods less rewarding over time.
This change is associated with a reduction in neurotensin, an important chemical messenger in the brain. The discovery may pave the way for new strategies to combat obesity, aiming to restore the function of this brain system.
READ MORE:
Changes in neurotensin signalling drive hedonic devaluation in obesity
Neta Gazit Shimoni, Amanda J. Tose, Charlotte Seng, Yihan Jin, Tamás Lukacsovich, Hongbin Yang, Jeroen P. H. Verharen, Christine Liu, Michael Tanios, Eric Hu, Jonathan Read, Lilly W. Tang, Byung Kook Lim, Lin Tian, Csaba Földy & Stephan Lammel
Nature (2025).
Abstract:
Calorie-rich foods, particularly those that are high in fat and sugar, evoke pleasure in both humans and animals1. However, prolonged consumption of such foods may reduce their hedonic value, potentially contributing to obesity2,3,4. Here we investigated this phenomenon in mice on a chronic high-fat diet (HFD). Although these mice preferred high-fat food over regular chow in their home cages, they showed reduced interest in calorie-rich foods in a no-effort setting. This paradoxical decrease in hedonic feeding has been reported previously3,4,5,6,7, but its neurobiological basis remains unclear. We found that in mice on regular diet, neurons in the lateral nucleus accumbens (NAcLat) projecting to the ventral tegmental area (VTA) encoded hedonic feeding behaviours. In HFD mice, this behaviour was reduced and uncoupled from neural activity. Optogenetic stimulation of the NAcLat→VTA pathway increased hedonic feeding in mice on regular diet but not in HFD mice, though this behaviour was restored when HFD mice returned to a regular diet. HFD mice exhibited reduced neurotensin expression and release in the NAcLat→VTA pathway. Furthermore, neurotensin knockout in the NAcLat and neurotensin receptor blockade in the VTA each abolished optogenetically induced hedonic feeding behaviour. Enhancing neurotensin signalling via overexpression normalized aspects of diet-induced obesity, including weight gain and hedonic feeding. Together, our findings identify a neural circuit mechanism that links the devaluation of hedonic foods with obesity.
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