by Sanjukta Mondal , Medical Xpress
VTA dopamine-releasing neurons control appetite during food consumption. Credit: Science (2025). DOI: 10.1126/science.adt0773
Delicious and extremely palatable food can increase the tendency of hedonic eating, where one consumes food for the sole purpose of deriving pleasure instead of the body’s energy needs. Hedonic eating often leads to eating beyond satiety (fullness), which is linked to obesity. Although food palatability is closely linked to hedonic eating, the neural mechanisms underlying this process remain largely unclear.
A recent study on mice by researchers from the University of California, San Diego and Howard Hughes Medical Institute, Ashburn, identified a brain circuit between the peri-locus coeruleus and the ventral tegmental area (VTA) responsible for driving increased consumption of palatable food. The work is published in the journal Science.
The VTADA or dopamine neurons in VTA, also called the brain’s reward center, decided the palatability of food and played a key role in driving hedonic eating behaviors and reducing the effectiveness of obesity medications.
Eating behaviors progress in three distinct phases: seeking (initiation), consumption (sustaining), and satiety (terminate feeding). Using cell-specific circuit mapping and optogenetics—a biological technique for controlling neurons or cell activity with light—the researchers found that the dopamine neurons in VTA did not impact the food-seeking behavior.
They were only triggered during food consumption, and their activity increased or decreased in response to the tastiness of the food. The researchers noted that activating the neurons with optogenetics during eating prolonged food intake, similar to the effect of making food more palatable, but inhibiting these neurons reduced consumption without affecting the initiation of eating.
The activity of the dopamine neurons during the consumption of food was suppressed by semaglutide, a glucagon-like peptide receptor 1 (GLP-1R) agonist that mimics the brain’s satiety signals and is commonly used as an antiobesity drug.
Mice treated with semaglutide ate less and exhibited low VTADA neuron activity; however, artificially activated neurons during food consumption overcame the appetite-reducing effect of semaglutide and enhanced both food intake and eating duration.
The researchers noticed that as mice lost weight on semaglutide, VTADA neuron activity increased, and so did the intake of palatable food. This observation could help explain why some obesity medications containing semaglutide fail to completely suppress overeating in certain individuals. They also found that this anti-semaglutide behavior can be effectively reversed by targeted inhibition of VTADA neurons.
The mechanism by which VTADA neurons regulate the duration of food intake provides key insights into how palatable food influences appetite. Exploring the interactions between these neurons and different parts of the brain could open up new avenues for developing strategies to combat obesity and other metabolic disorders.
More information: Zhenggang Zhu et al, Hedonic eating is controlled by dopamine neurons that oppose GLP-1R satiety, Science (2025). DOI: 10.1126/science.adt0773
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