International Business Department           Liu Bojia           March 31, 2025

  Have you ever had a full meal and still couldn't resist a slice of cake or a cup of milk tea? Even though you are no longer hungry, you still want to try more food. This type of eating behaviour, which is driven by the taste of food rather than by physiological needs, is known as hedonic eating, and is less dependent on the body's need for energy and more influenced by the appeal of the food itself. Excessive hedonic eating is strongly associated with obesity, bulimia and various metabolic diseases.

  But how does the brain translate taste into a ‘one more bite’ command? Past research has suggested that dopamine, which is closely linked to pleasure and reward mechanisms, plays an important role in hedonic eating. However, this idea remains controversial in the field, as studies have found that activating dopamine neurons reduces an individual's food intake, which contradicts the hypothesis that dopamine promotes eating.

  To further clarify the relationship between dopamine and eating, a team of researchers from the University of California, San Diego, designed a more precise experiment: instead of activating or inhibiting dopamine neurons in general, they intervened only when the animals were eating. As a result, they found that dopamine neurons located in the ventral tegmental area (VTA) were activated upon the perception of a tasty meal and released dopamine to produce a sense of pleasure.

  What's even more refreshing is that these neurons can effectively control the length of time an individual eats! In other words, when they are activated, an individual will have a constant urge to eat, so you can't help but keep consuming more and more delicious food. A related research paper has been published in the journal Science.

  In the experiment, the researchers provided mice with different foods with high and low levels of deliciousness and monitored the activity of the mice's VTA dopaminergic neurons in real time while they were eating. The results showed that the activity level of VTA dopaminergic neurons was highly correlated with the duration of feeding; when the mice licked the high-delicious food, the neuronal activity continued to increase, and the mice spent more time eating; whereas the activity triggered by the low-delicious food was weaker, and the mice soon stopped eating. In other words, the tastier the food, the stronger the dopamine signals and the longer it took to eat.

  Even more amazingly, it is possible to artificially control the mice's feeding behaviour and timing by simply modulating the activity of VTA dopaminergic neurons. For example, if VTA dopamine neurons were activated precisely when mice were eating low-tasting food, mice that were not interested in low-tasting food significantly extended their eating time, and their behavioural pattern became similar to that of high-tasting food; and if neuronal activity was inhibited in the opposite direction, the high-tasting food would pale in comparison to that of the mice.

  In addition, the action of VTA dopaminergic neurons is highly specific. If these neurons are activated in mice in a non-feeding state, they are not prompted to search for food or increase food intake. This suggests that VTA dopaminergic neurons do not simply promote appetite, but influence hedonic eating by regulating the ‘persistence’ of eating.

  In the study, the authors also found another related type of periplasmic glutamatergic neuron. It inhibits the activity of VTA dopaminergic neurons and is therefore a type of neuron that reduces hedonic eating.

  Of interest, the team also tested the effects of the popular diet drug of the moment, a GLP-1 receptor agonist, on hedonic eating. They tried injecting mice with simethicone and then analysed the mice's response to highly tasty food. The results showed that simethicone reduced the activity of VTA dopaminergic neurons during feeding, which reduced the mice's interest in the food and shortened the duration of the meal.

  However, with the prolonged administration of the drug, the activity of VTA dopaminergic neurons gradually recovered after the mice lost weight, and their intake of high-tasting food rebounded. This ‘rebound effect’ can be reversed by optogenetically inhibiting the dopamine neurons. This finding provides new insights into the limitations of the efficacy of simethicone: the drug reduces hedonic eating by inhibiting VTA dopaminergic neuron activity, but the reactivation of the neurons may be the underlying cause of weight regain.

  This study not only reveals the neural mechanisms of hedonic eating, but also provides new ideas for obesity treatment. Traditionally, dopamine is mainly associated with ‘wanting to eat’, but this study demonstrates that it also directly controls ‘how long to eat’. Targeting VTA dopaminergic neurons is expected to block the excessive desire for food, and may also be able to treat obesity in combination with drugs such as simethicone.