Hunger-Blocking-Übungsmolekül treibt Gewichtsverlust ohne Training | Während die Entdeckung bei Mäusen gemacht wurde, hat sie das Potenzial, eine neue Möglichkeit für das Gewichtsmanagement zu sein, der nicht mit der Art von Magen -Darm -Stress von Arzneimitteln verbunden zu sein scheint.

From the article: Scientists have found out exactly how an exercise-triggered molecule suppresses hunger signals in the brain, leading to weight loss. And the good news is that it could be harnessed as a therapeutic, providing the same benefits without the hard work it takes to produce it naturally.

Researchers led by scientists at Baylor College of Medicine (BCM) have [unraveled](https://www.nature.com/articles/s42255-025-01377-9) just how an exercise-induced signaling metabolite, N-lactoyl-phenylalanine (Lac-Phe), travels a unique pathway to the brain and impacts the activity of one, and then two different neurons. It triggers a chain of events that ultimately suppresses appetite – something we’ve known Lac-Phe can do, but until now we didn’t know just how.

“Regular exercise is considered a powerful way to lose weight and to protect from obesity-associated diseases, such as diabetes or heart conditions,” said co-corresponding author Dr. Yang He, an assistant professor at BCM. “Exercise helps lose weight by increasing the amount of energy the body uses; however, it is likely that other mechanisms are also involved.

“Understanding how Lac-Phe works is important for developing it or similar compounds into treatments that may help people lose weight,” he added. “We looked into the brain as it regulates appetite and feeding behaviors.”

Lac-Phe is the metabolite that’s most increased after intense bouts of exercise, and it’s seen in humans, mice and racehorses. The researchers previously found that giving added Lac-Phe to mice reduced their food intake without any negative side effects, showing that the signaling molecule still worked as if the body had produced it naturally through exercise.

In this latest work, the team looked at two brain cells in mice – agouti-related peptide (AgRP) neurons in the arcuate nucleus of the hypothalamus, which stimulate hunger, and paraventricular nucleus (PVN) neurons in the paraventricular nucleus of the hypothalamus, which help dial down hunger signals. The two neurons form a system where AgRP neuronal signals inhibit PVH neurons, activating hunger. But when AgRP neurons are switched off, PVH neurons become more active, suppressing appetite.

Lac-Phe, the team discovered, directly blocks AgRP neurons – which boosts the activity of the PVH neurons – via a specific ATP-sensitive potassium channel (KAPT channel).