The circuitry in the brain may be blamed for overeating and consuming more tasty food than what is actually needed by the body.
Scientists from the University of North Carolina School of Medicine identified a specific network of cellular communication in the brain of mice that acts as motivator to keep eating palatable food. These cells are located within the central amygdala in the brain's emotion-processing region.
The amygdala is linked to pain and anxiety and fear. The findings highlight that the amygdala also regulate pathological eating.
Switch In The Brain
The prepronociceptin-expressing cells within the amygdala are specifically responsible for craving palatable foods.
This mammalian circuit in the brain is not due to inherent gluttony but a product of evolution. The brain was wired to consume as much calorie as humanly possible to stock up on extra energy because no one knew when the next meal would be available. It was a way to adapt during ancient times when famines were frequent.
"This circuit seems to be the brain's way of telling you that if something tastes really good, then it's worth whatever price you're paying to get to it, so don't stop," said Thomas Kash, Ph.D., a distinguished professor at the UNC.
Homeostatic And Hedonistic Feeding
The search for anti-obesity remedies led scientists to study brain cells and circuits involved in ordinary, "homeostatic" feeding. Homeostatic feeding is triggered by hunger and it keeps the body's energy level up.
More recently, some scientists have been studying "hedonic" feeding or the pleasure-driven eating of calorie-rich food that is way beyond the body's energy needs.
According to Kash, following this instinct now when there is plenty of calorie-rich foods, can lead to obesity and related medical conditions such as diabetes, heart disease, and cancers.
Turning Off The Switch
In the study, the scientists engineered mice to produce a fluorescent molecule along with nociceptin to illumine the cells that drive nociceptin circuits. One of the multiple nociceptin circuits in the brain became active when the mice got a chance to binge on calorie-rich food.
The scientists deleted about half of the nociceptin-making neurons in the circuit and observed that it reduced the mice's binge-eating when they had access to rich food, without affecting their intake of ordinary food.
"In the study, we find that when we take these neurons away we get reduced consumption of palatable foods, arguing that these neurons are necessary for tasty food consumption,” said Andrew Hardaway, Ph.D., a research assistant professor at the UNC.
The UNC team are now studying how this circuit works in relation to feeding and other factors, and how nociceptin antagonists can alter its functions.
