It’s no secret that consuming energy-dense foods consistently promotes weight gain. However, when Stephanie Borgland at the University of Calgary gave rats unrestricted access to high-fat, high-sugar foods, the rodents not only got fat, their brains changed too. The food essentially rewired their brains, inducing the rodents to crave more of the same food, even when their hunger should have been satisfied.
Borgland and colleagues fed rats a the so-called “cafeteria diet”, which, besides the regular “rat chow” (a balanced diet), consists of unlimited access to food rich in fat and sugar, such as chocolate and other treats. Freely left to eat any food and as much as they wished from the 24h/day cafeteria diet, the rats became obese in only 40 days. However, rats that had limited access to the energy-dense diet (one hour per day), did not become obese.
“Eating an energy dense diet can change circuits in your brain to make you want to eat more. This is not food addiction, but probably a natural mechanism to help you maximize opportunities to eat when presented with energy dense (typically palatable) food,” Borgland told ZME Science.
Previously, work carried out by the same team of researchers had shown that obese mice have modifications in signaling in a brain region called the orbitofrontal cortex (OFC), which is located right above the orbits of the eyes. This brain region is associated with decision-making and receives information from the senses in order to register the value of the food, then updates feeding behavior based on this information. For instance, delicious-smelling food relayed to the OFC by the sense of smell might promote a more enthusiastic appetite.
In non-obese animals, satiety leads to food devaluation, which reduces appetite. Conversely, obese animals show a reduction in the inhibitory signals on a class of neurons called pyramidal neurons, found in the OFC. In other words, the obese rats feel less full even though they should be.
The new study identified endocannabinoid signaling as a key component in this modification, which was a very exciting discovery.
“Obesity is typically associated with an elevated level of endocannabinoids in both humans and rodents, so these results are not surprising,” Borgland said in a statement. “However, endocannabinoid signaling is much more complex than previously thought. Our research shows that endocannabinoid signaling selectively affects inhibitory signals onto the pyramidal neurons of the OFC. This effect is mediated through changes in specific receptors on the neurons, but may also involve other types of cells in the brain, called astrocytes,” the researcher added.
Since 1975, obesity rates around the world have tripled, today leading 13% of the adult population to be classed as obese. Obesity is a serious concern because it is associated with poorer mental health outcomes, reduced quality of life, and the leading causes of death in the U.S. and worldwide — including diabetes, heart disease, stroke, and some types of cancer.
“Future studies will need to further investigate the mechanisms through which endocannabinoids affect the motivation to eat beyond satiety. This will be critical in identifying novel therapeutic strategies for treating obesity with fewer side effects” concludes Dr. Borgland.
The findings were presented at the 12th Annual Canadian Neuroscience Meeting.