Ghrelin Hormone Controls Stress-Caused High-Calorie Junk Food Intake

People who suffer from high stress and depression tend to eat more high fat foods. This, in turn, makes them fatter. Though this fact was more or less known by many people, the underlying mechanisms that are ultimately controlled by the brain circuits remained unclear so far. This current study reported an interesting mouse model that mimicked the effects of extended psychosocial stress and severe depression in humans. They showed that stress caused the mice to produce more of a hormone called ghrelin in the circulation. Ghrelin then binds to its receptors in the brain, minimizing the depressive behavior while provoking the brain to eat high calorie foods. This of course has obvious harmful effects like an increase in obesity. Researchers proved this model in stressed-out mice and suggested that a similar phenomenon would occur in highly stressed humans as well.
People under stress and depression often undergo a change in their food intake pattern, either eating more or less than usual. Typically, they become addicted to eat high fat junk foods, which results in increased obesity. Several past studies have demonstrated such correlation between stress and obesity among humans. This was especially relevant for affected U.S. soldiers. There are also reports that stress causes an increase in hormone ‘ghrelin’ in stomach for both humans and mice. Few mouse models also showed that if ghrelin was injected the mouse chose the tastier and calorie rich peanut butter and sucrose pulps in the menu. But this behaviour was absent in mice that were devoid of functional ghrelin receptors. However, all of these studies were limited by giving an exact animal model that will give us the molecular connections between stress, ghrelin, high-fat food intake, and obesity. The present evaluation put together the missing pieces and gave a complete road map.
* Male mice with or without the ghrelin receptors were fed a regular chow and water diet.
* Test mice were introduced to a social competitive stress for 10 days, during which they were allowed to fight with more aggressive and older mice. A period of isolation for any interaction with unknown mice followed, which caused them both stress and depression. Meanwhile, the control mice were not exposed to any stress and isolation. Blood hormone levels were monitored after the stress period.
* Thereafter, mice were allowed to choose between the regular and high fat diets. The food intake was also observed for normal mice with or without injected ghrelin.
* The brains were extracted and the RNA (one of the three major macromolecules along with DNA and proteins) of ghrelin receptors was studied
* Histochemical study (study of the microscopic anatomy of cells and tissues) was performed on brain sections and neurons were pictured in mice with or without the ghrelin receptors.
* Statistical analyses determined the association between stress, ghrelin levels, food intake and obesity.
* Both mice who underwent social competitive stress and mice who were injected with ghrelin took high calorie food. The control mice and the mice without ghrelin receptors took normal diet (group 2).
* Group 1 mice that ate more calorie diet gained more weight when compared to group 2 mice with a normal diet.
* Direct ghrelin signaling via ghrelin receptors localized to certain brain neurons was sufficient for both ghrelin-mediated anti-depressantactions and tasty, high-calorie food intake behavior.
Shortcomings/Next steps
“Although the current study does focus in on the identity of those neurons that are sufficient for ghrelin’s actions in coordinating the response to stress… did not allow us to further narrow down the site of direct ghrelin action to one particular brain nucleus.” The authors claimed that a more sophisticated experimental design may pinpoint a particular brain area for ghrelin’s action. “It is also intriguing to speculate whether the mechanisms herein described for stress-associated food-reward behaviors may be generalized to other reward behaviors known to occur in the setting of psychosocial stress.” Here the authors suggested that further experiments could show an association between stress and drug addiction, too. The authors believe that more research should be performed to answer some relevant questions including the role of other hormone and neuron signaling in the current perspective.
The mouse model described here is unique as it can easily be related to prolonged human stress and depression. The competitive social stress in mice increases the ghrelin hormone levels in their circulation. When ghrelin hormone binds to its receptors in certain brain neurons (like ventral tegmental area neurons), the mice feel less depressed and feel like taking more junk foods that could give them more pleasure. Consequently they become more obese. The role of ghrelin hormone in tempting them for taking high fat food is confirmed by the fact that absence of functional ghrelin receptors result in neither junk food intake nor weight gain. This is the first report where the ghrelin receptor expression was conditionally controlled in mice and we could know that ghrelin receptor expression in which types of neurons in brain are responsible for ghrelin-induced behavior. Finally,the model could prove extremely valuable for developing pharmaceutical drugs to stop the temptations for the junk food and any possible weight gain.
For More Information:
Ghrelin Mediates Stress-Induced Food-Reward Behavior in Mice
Publication Journal: Journal of Clinical Investigation
Jen-Chieh Chuang, Mario Perello, Ichiro Sakata,; University of Texas Southwestern Medical Center, Dallas, Texas
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