Dopamine neurons that the supercharged fuel can weaken the effectiveness of obesity drugs

Delicious and extremely pleasant foods can increase the trend of hedonic food, where food is eaten for the sole purpose of drifting pleasure instead of the body’s energy needs. Hedonic food often leads to eating beyond satiety (fullness), which is linked to obesity. Although the palatability of food is closely linked to hedonic food, the neural mechanisms underlying this process remain largely clear.

A recent study on mice by researchers from the University of California in San Diego and Howard Hughes Medical Institute, Ashburn, identified a cerebral circuit between the Coeruleus de Péri-Locus and the Tegmental Ventral (VTA) area responsible for the increased consumption of appetissable food. The work is published in the journal Science.

VTA^DA Or the dopamine neurons in VTA, also called the brain reward center, have decided to palate food and have played a key role in driving hedonic eating behaviors and the reduction in the effectiveness of obesity drugs.

Food behavior is progressing in three distinct phases: research (initiation), consumption (maintenance) and satiety (finish food). Using the mapping of specific cells and optogenetics – a biological technique to control neurons or cellular activity with light – researchers have found that dopamine neurons in VTA have not had an impact on food research behavior.

They were only triggered during food consumption, and their activity increased or decreased in response to the flavor of food. Researchers noted that activation of neurons with optogenetics during consumption of prolonged food consumption, similar to the effect of making food more pleasant to taste, but inhibiting these neurons reducing consumption without affecting the initiation of the food.

The activity of dopamine neurons during food consumption was removed by semaglutide, an agonist of the Glucagon type peptide receptor (GLP-1R) which imitates brain satiety signals and is commonly used as an anti-American medication.

Mouses treated with semaglutide have eaten less and showed a weak VTA^DA neurons activity; However, artificially activated neurons during food consumption have overcome the effect of reduction of semaglutide appetite and improved both food intake and the duration of the food.

The researchers noticed that as mice, the mice lost weight on the semaglutide, VTA^DA The activity of neurons has increased, as is the consumption of pleasant food for taste. This observation could help explain why certain obesity drugs containing semaglutide fail to completely remove the overeating in some people. They also found that this anti-semaglutide behavior can be effectively reversed by the targeted inhibition of VTA^DA neurons.

The mechanism by which VTA^DA Neurons regulate the duration of food consumption provides essential information on how appetizing food influences appetite. The exploration of interactions between these neurons and different parts of the brain could open new ways to develop strategies to combat obesity and other metabolic disorders.

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