Such an approach could offer a way to treat obesity as well
People with Prader Willi syndrome, a genetic disorder, have an insatiable appetite. They never feel full, even after a hearty meal. The result can be life-threatening overeating and obesity.
According to a new study, their constant hunger results in part to disordered signaling in the brain’s cerebellum, a region of the brain also responsible for motor control and learning.
An international research team spanning 12 institutions used clues from Prader Willi patients to guide investigations in mice that uncovered a subset of cerebellar neurons that signals satiation after eating.
The work, shared in the journal Nature, suggests that neurons in the cerebellum’s anterior deep cerebellar nuclei (aDCN) are involved in helping animals regulate their meal size.
Zeroing in on a subset of aDCN neurons shown to be activated by feeding, the research team dug deeper into the neurons’ role in regulating hunger and satiety. In hungry animals, these neurons turned on quickly and strongly upon being given food; in fed animals, the neurons remained quiet.
Researchers aim to continue filling in the details about the regulatory control of hunger, contributing to a more complete overall picture of how hunger and satiety are regulated in the brain.