Summary: Researchers uncovered a brain molecule’s role in triggering comfort food cravings after experiencing stress. Their research reveals that the molecule Proenkephalin, located in the hypothalamus, is crucial in inducing overeating following a stressful event.
By exposing mice to a natural predator’s odor and observing their response, the team demonstrated that this molecule activates neurons sensitive to high-fat food consumption.
This discovery not only provides insights into the mechanisms of emotional eating but also suggests potential therapeutic targets to address stress-induced overeating.
The study identified the molecule Proenkephalin in the hypothalamus as key in linking stress to overeating.
Experiments showed that activating neurons expressing this molecule led to overeating behavior in mice.
This research offers a potential therapeutic target for alleviating emotionally triggered eating.
Source: Virginia Tech
If you’ve had a near miss accident in your car or suffered the intimidation of a menacing person, you’ve probably felt it — a psychological reaction to a threat called a fight or flight response. Your heart rate climbs, anxiety washes over you, you might shake or sweat.
But hours after that stress passes, you may feel another response — a powerful desire for comfort food, that highly processed, high-fat stuff you know isn’t good for you. It can relieve stress and tension and provide a sense of control. Emotional eating following a stress-triggering interaction is familiar to many of us, and to scientists as well.
But how a threat signals your brain to want comfort food has been unknown.
Now, a Virginia Tech scientist has pinpointed a molecule found in a region of the brain called the hypothalamus that is connected to changes in the brain that lead to emotional overeating. Sora Shin, assistant professor at the Fralin Biomedical Research Institute at VTC, and her research team described the discovery in a paper published Oct. 28 in Nature Communications.
“We don’t always eat because we are hungry and we have certain physical needs,” said Shin, who is also an assistant professor in the Department of Human Nutrition, Foods, and Exercise in Virginia Tech’s College of Agriculture and Life Sciences. “Whenever we get stressed or feel some threat, then it can also trigger our eating motivation. We think this molecule is the culprit.”
Shin and her research team began their study by investigating a small molecule, Proenkephalin. This molecule is common in multiple parts of the brain, but little research had examined its role in the hypothalamus. Shin suspected it played a role in stress and eating because the hypothalamus is a center for regulating eating behavior.
The lab exposed mice to the odor of cat feces. The odor of a natural predator triggered a threat response in the mice, and 24 hours later, the mice exhibited a negative emotional state, overeating behavior, and neurons in their brains showed sensitivity to consumption of high-fat foods.
To confirm the role of the molecule in stress-induced eating, the researchers activated the same neurons artificially with light stimulating a genetically encoded molecule expressed in the neuronal cell’s membrane, without the predator scent, and saw a similar response.
In addition, when they exposed the mice to the cat odor and quieted the reaction of the neurons expressing that molecule with the same technique, the mice showed no negative emotional state and didn’t overeat.
“So something about this molecule itself is very critical to inducing overconsumption after the threat,” Shin said.
The discovery points toward a possible target for therapy to alleviate emotionally triggered eating.
“We have much more to learn about this molecule,” Shin said, “but we found its location and it could be a good starting point.”
Shin’s first-authors on the study are In-Jee You, a former research associate at the institute, and Yeeun Bae, a human nutrition, foods, and exercise graduate student working in her lab.
About this stress research news
Author: John Pastor Source: Virginia Tech Contact: John Pastor – Virginia Tech Image: The image is credited to Neuroscience News
Lateral hypothalamic proenkephalin neurons drive threat-induced overeating associated with a negative emotional state
Psychological stressors, like the nearby presence of a predator, can be strong enough to induce physiological/hormonal alterations, leading to appetite changes. However, little is known about how threats can alter feeding-related hypothalamic circuit functions.
Here, we found that proenkephalin (Penk)-expressing lateral hypothalamic (LHPenk) neurons of mice exposed to predator scent stimulus (PSS) show sensitized responses to high-fat diet (HFD) eating, whereas silencing of the same neurons normalizes PSS-induced HFD overconsumption associated with a negative emotional state.
Downregulation of endogenous enkephalin peptides in the LH is crucial for inhibiting the neuronal and behavioral changes developed after PSS exposure.
Furthermore, elevated corticosterone after PSS contributes to enhance the reactivity of glucocorticoid receptor (GR)-containing LHPenk neurons to HFD, whereas pharmacological inhibition of GR in the LH suppresses PSS-induced maladaptive behavioral responses.
We have thus identified the LHPenk neurons as a critical component in the threat-induced neuronal adaptation that leads to emotional overconsumption.