The process of eating is regulated by a relatively simple brain circuit, consisting of three different types of neurons that connect the hunger hormone with the jaw, thus stimulating chewing movements. An investigation conducted on mice by researchers at Rockefeller University in New York has revealed these mechanisms, with results published in the journal Nature. These studies suggest that the desire to eat may be more like an automatic reflex rather than a deliberate process, offering new insights into how eating behavior is triggered.

Led by geneticist Jeffrey M. Friedman, the research examined a particular area of ​​the brain associated with glucose regulation and appetite: the ventromedial hypothalamus. This region is known to play a crucial role in weight management, as damage to it can lead to obesity. Within this area are neurons that produce the protein BDNF (brain-derived neurotrophic factor). When these neurons are inhibited, food intake increases significantly (up to 1,200 percent more) and chewing movements are activated even in the absence of food or sensory cues that would indicate that eating time has arrived. Conversely, when these neurons are stimulated, food intake decreases and chewing movements are blocked.

By mapping signals to and from BDNF neurons, the researchers identified a three-component neural circuit that links hormonal signals of appetite to the movements needed to eat. At one end of this circuit are neurons in the arcuate nucleus of the hypothalamus that are responsible for receiving hunger signals, such as the hormone leptin produced by fat cells. These neurons send information to BDNF neurons in the ventromedial hypothalamus, which in turn communicate with neurons in a region of the brainstem called Me5. This center controls the jaw muscles and also appears to be involved in stress-related oral compulsive behaviors, such as chewing on objects or hair.