People who Wegovy and take similar weight loss medication often feel full, even if they sit down and have not taken a single bite. Now scientists have discovered a brain region that is involved in this effect-and which contributes to the same sensation without using Delivery medication.

in a Today in Science 1 describe two groups of neurons with are related to the feeling of satiety: one for the feeling of precaution and one for the feeling of follow -up. The study also shows that The blockbuster acceptance medication act on the 'saturation' neurons, but further examinations are required to determine the mechanism of action of the treatments, say the authors.

The identification of these two neuron populations is the main contribution of the work, says Allison Shapiro, a neuro development at the University of Colorado Anschutz Medical Campus in Aurora, which was not involved in research. It fits the anecdotal idea that there are two types of saturation: one that is anticipating, and another that arises in response to the food. "Based on what you have found, it seems that this specific area of ​​hypothalamus is responsible for both, which is pretty cool."

saturation without food

The latest obesity medication Ahmen a hormone called glucagon-like peptide 1 (GLP-1), which controls the blood sugar level and acts on the brain to curb the appetite. The GLP-1 medication includes Semaglutid, which is sold as an Ozempic for type 2 diabetes (T2D) and as a Wegovy for weight loss, and Liraglutide, which is sold as a saxenda for weight reduction and as victoza for T2D. Both are made by Novo Nordisk, based in Bagsværd, Denmark.

The study mitutor Hyung Jin Choi, a neuroscientist at Seoul National University, experienced the effects of Liraglutid first -hand when he took the medication against obesity. "I felt an enormous increase in saturation when I saw and smelled food before I started eating," he says. This motivated him to dive deeper into the feeling of pension.

he and his colleagues recruited people with obesity and asked them to report their satiety in three stadiums: before contact with food; at the sight of a delicious plate of Korean fried chicken, but before eating; And after eating. People who took Liraglutid felt full before contact with food, but this feeling reinforced when they were shown food and again after they had eaten. The results show that Choi is not the only one who, in contrast to the participants who do not take the medication, is already fed up with the mere sight of Essen. A feeling that the team called 'Prandial saturation'.

In contrast, in contrast to participants who did not take the medication, the saturation at sight of the fried chicken and only climbed again after eating.

In order to identify the area of ​​the brain, which is responsible for these sensations, the researchers focused on the dorsomedial hypothalamus (DMH). Its neurons have GLP-1 receptors that enable GLP-1 to act directly on this brain area.

The researchers artificially stimulated the DMH neurons in mice that were in the middle of a meal and found that the animals stopped eating immediately. When these neurons were chronically activated, the mice ate less; When they were chronically inhibited, the mice ate more. The results suggest that the area plays a central role in saturation.

neurons that signal 'I am full'

After this was found, the authors examined the activity of individual neurons in the mouse's DMH. They identified two neuron populations: one that was continuously active from the moment the mice started looking for food, until the time they started eating, and another who was only active than eating the mice.

The authors also showed that GLP-1 medication act on the DMH. In mice that Liraglutid received, the neural activity in this brain region was higher before and during meals than in mice that the medication had not received. The team deleted GLP-1 receptors in the DMH neurons of some animals, which inhibited Liraglutid's ability to work on this brain area. The mice ate more than those with functioning GLP-1 receptors, which indicates that Liraglutid's ability to suppress the appetite was weakened.

Karolina Skibicka, a neuroscientist at Penn State in University Park and the University of Gothenburg, Sweden, notes that other studies have observed no such changes in the eating behavior after manipulation of GLP-1 receptors in this brain area 2 . A possible explanation could be related to the two neuron populations discovered in the DMH. "We tend to view GLP-1-receptor-expressive neurons in a certain brain area as a homogeneous population that all play the same role," she says. "This work shows that this is obviously not the case. It is just a brain area, but GLP-1 receptors on neurons do different things there."

The study showed a congruence between what was observed in humans and mice, says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia, Pennsylvania. She notes that it is becoming increasingly important to involve clinical observations in basic research on GLP-1 medication. "But then it is also important to go back and then to confirm the existence of these mechanisms in humans. This work was a nice example that it goes in both directions."