Constant hunger associated with Prader-Willi syndrome is, in part, the result of disordered signaling in the cerebellum, an area of the brain associated with motor control and learning.
The brain regulates both eating for hunger and pleasure through serotonin-producing neurons in the midbrain, but the different types of feeding are wired by independent circuits that do not influence the other type of feeding.
Researchers have identified a subpopulation of dopaminergic neurons in the caudal ventral tegmental area that appears to suppress food intake by triggering satiation in mice.
Study sheds new light on how the brain regulates hunger. The findings may help with the development of new drugs to fight obesity.
A new study reveals people who experience larger dips in blood sugar hours after eating end up feeling hungrier and eat hundreds of more calories a day than those who experience lower blood sugar dips.
Researchers have identified novel neurocircuitry between midbrain structures which are modulated by leptin to control eating behaviors in mice.
Higher levels of the hunger hormone ghrelin predict a greater preference for smaller, immediate financial rewards over larger, delayed financial rewards.
During vigorous exercise, the body produces large amounts of the hormone GDF15, but the quantity is not sufficient enough to affect behavior or appetite.
Activity in the substantia nigra is similar following a day of social isolation as it is following a day of starvation.
The hunger hormone ghrelin doesn't just influence where and when animals eat, it also appears to have an impact on memory. Disrupting signaling of ghrelin to the vagus nerve caused rats to forget they had just eaten, even though the animals remembered they had just had access to food. Findings suggest disrupted ghrelin signaling could negatively impact episodic memory.