It’s common knowledge that diets high in fat and sugar lead to obesity, but according to a new study, they also cause changes in the brain that inhibit the feeling of being full.
Researchers from the University of Calgary found that rats with unrestricted access to unhealthy foods not only caused an increase in obesity in the rats, but also caused brain changes that made the food more attractive to them.
The unhealthy foods led to modifications in the endocannabinoid signaling in a brain region called the orbitofrontal cortex (OFC).
According to the World Health Organization (WHO), obesity has tripled since 1975. In 2016, nearly 13 percent of adults worldwide were obese.
More and more studies have found that obesity is a major risk factor for cardiovascular disease, some cancers, and disorders like osteoarthritis. Studies like this most recent one from the University of Calgary adds to the body of work being done to better understand the mechanisms that drive obesity.
For the study, the researchers gave a group of rats the cafeteria diet, which allows rats unrestricted access to high-fat, high-sugar foods like chocolate in addition to their regular meals of “rat chow,” or the balanced diet rats typically get.
After 40 days of the cafeteria diet, the rats became obese while another group of rats with limited access to the sugary treats did not.
Previously, it was found that obesity resulted in changes in the signaling in a brain region called the Orbitofrontal Cortex (OFC) and the researchers wanted to examine these changes more in depth.
The OFC is the part of the brain that helps with decisions making and receives food information from the senses. After food information from the senses is sent to the OFC, value is assigned to the different foods.
For non-obese animals, satiety leads to food being devalued in the OFC and motivation to eat is decreased. In obese animals, the researchers discovered that endocannabinoid signaling in the OFC reduces the “stop” signals in the brain.
“Obesity is typically associated with an elevated level of endocannabinoids in both humans and rodents, so these results are not surprising,” said Stephanie Borgland, the leader of the research. “However, endocannabinoid signaling is much more complex than previously thought. Our research shows that endocannabinoid signaling selectively affect 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.”
With obesity increasing more than waistlines, understanding what modifications in the brain can drive weight gain is critical for reducing the health risks associated with obesity.
“Future studies will need to further investigate the mechanisms through which endocannabinoids affect the motivation to eat beyond satiety,” said Borglan. “This will be critical in identifying novel therapeutic strategies for treating obesity with fewer side effects.”