When hunger strikes, simply seeing a picture of a cheeseburger or a pizza may be enough to get you running to the nearest diner. But if you’re still tempted by these visual cues after eating a large meal, a new study suggests that it may be down to faulty brain wiring, rather than a lack of willpower.
Researchers from the Beth Israel Deaconess Medical Center (BIDMC) in Boston, MA, have uncovered how neurons in the insular cortex of the brain influence how we respond to food cues.
What is more, the researchers found that it may be possible to control the activity of these neurons and alter eating habits, a discovery that could lead to new treatment strategies for eating disorders and obesity.
Study co-author Mark Andermann, Ph.D., of the Division of Endocrinology, Diabetes and Metabolism at BIDMC, and colleagues recently reported their findings in the journal Nature.
Previous studies have suggested that the insular cortex affects our behavior in response to food cues, such as food-related television commercials.
The researchers explain that in healthy individuals who are hungry, activity in the insular cortex increases in response to food cues, but it does not increase in response to such cues after a large meal.
However, brain imaging studies have indicated that individuals who are obese or have eating disorders may possess abnormalities in the insular cortex that increase their sensitivity to food cues, which may explain why some people overeat.
Studying the insular cortex of mice
For their study, Dr. Andermann and colleagues set out to gain a better understanding of the brain activity that influences eating behavior in response to food cues.
To reach their findings, the researchers studied the insular cortex of mouse models.
In mice, the insular cortex is hard to reach, but Dr. Andermann and team developed a tiny periscope that allowed them to assess neuronal activity within this brain region.
Using this novel tool, the researchers analyzed neuronal activity in the rodents’ insular cortex in response to food cues in two conditions: when they were hungry and when they were sated.
The team found that when the mice were hungry, food cues led to the activation of a group of neurons in the insular cortex that influenced food-seeking behavior. When the mice were sated, however, these neurons were not activated.
Food-seeking behavior in sated mice triggered by ArGP neurons
Using genetic and optical techniques, the researchers then “switched on” neurons in the hypothalamus that express the gene for Agouti-related protein (AgRP). Activating these AgRP neurons promotes hunger.
The team found that activating the AgRP neurons not only caused sated mice to seek food in response to food cues, but it led to neuronal activity in the insular cortex comparable to that of hungry mice.
"These AgRP neurons cause hunger – they are the quintessential hunger neuron," says study co-author Dr. Bradford B. Lowell, also of the Division of Endocrinology, Diabetes and Metabolism at BIDMC.
"It's a major advance to learn that we can artificially turn them on and cause full mice to work to get food and to eat as if they hadn't eaten in a long time. These neurons seem capable of causing a diverse set of behaviors associated with hunger and eating."
The research also revealed that the brain pathway that connects AgRP neurons and the insular cortex involves the amygdala and paraventricular thalamus. The amygdala is involved in modifying the value of food cues, while the paraventricular thalamus plays a role in motivational behavior.
While further research is needed to gain a clearer understanding of the brain processes involved in behavioural responses to food cues, Dr. Andermann and colleagues believe that their current findings have therapeutic potential.
For example, the team suggests that it may be possible to reduce AgRP neuron activity in order to combat food cravings triggered by food cues, which may help to treat obesity.