Obesity has more than doubled worldwide since 1980. Currently, about 600 million people are considered obese and about two billion individuals are considered overweight. The factors that have caused this explosion are debatable, with evolving food trends, economic stressors and changes in the built environment ranking among the front-runners in terms of explaining the rise in obesity.
In recent years, research on obesity and overeating has ramped up, and scientists are gaining a more thorough understanding of what drives our eating habits.
Obesity occurs when our intake of energy from the food we consume exceeds our energy expenditure. Our food consumption is regulated by survival and reward, our pleasure senses (taste and smell) and demands from our body’s metabolism.
Cynthia Sass reported in Shape magazine that researchers in Italy have identified a specific type of pleasure-driven eating that they call hedonic eating. In a small study involving eight subjects, scientists found that eating for gratification, rather than for physiological hunger, triggers the release of hormones that increase appetite and therefore stimulate continued eating, even after physical satiety has been reached. In the study, blood levels of hunger hormones surged after eating cakes, but not after eating bread, butter or milk. While the connection isn’t completely understood, the hormonal reaction seems to occur with foods that are tied more closely to emotional, rather than physical hunger.
Recently researchers from the Johns Hopkins University School of Medicine have discovered, while studying the learning and memory system of the brain, a new type of nerve cell that appears to control feeding behaviors in mice. Their findings were published in the March 18, 2016 issue of Science.
“When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after,” Richard Huganir, director of the Department of Neuroscience at the Johns Hopkins University School of Medicine, said in a press release.
Huganir explains that his team’s discovery was a result of work on the proteins that strengthen and weaken the synapses between brain cells. Synapse strength is important in learning and memory and is an active research topic.
As part of their original research on synapse strength, Huganir and graduate student Olof Lagerlöf studied the enzyme O-linked N-acetylglucosamine transferase (OGT). The role of OGT is to add a molecule of N-acetylglucosamine to proteins, which alters the target protein’s behavior.
To learn about the role of OGT in learning and memory in the brain, which was his original area of interest, Lagerlöf deleted the gene that codes for it. Prior to examining the brain effect, he noticed that within the first three weeks the mice doubled in weight by building up their fat reserves. After careful observation of the eating habits of the mice, the researchers concluded that the absence of OGT interfered with the animals’ ability to sense that they were full.
“These mice don’t understand that they’ve had enough food, so they keep eating,” Lagerlöf said in a press release.
This was not the first study to highlight a neurological mechanism behind eating behavior. In 2015, researchers at the Rutgers Robert Wood Johnson Medical School published a study in Cell Reports describing that when the hormone glucagon-like peptide-1 (GLP-1) was reduced in the central nervous system of laboratory mice, the mice started to overeat and consume more high-fat food.
“The mice in which the GLP-1 deficiency was induced ate beyond the need for calories and showed an increased preference for high fat food,” Vincent Mirabella, coauthor of the study, said in a press release. “Conversely, when we enhanced GLP-1 signaling in the brains of mice we were able to block the preference of high fat foods.”
The authors discovered that activating the GLP-1 hormone in the mesolimbic system interfered with the communication between neurons, which exchange information to control reward behaviors such as eating. This resulted in the mice eating less food and losing their preference for foods high in fat.
“These are the same areas of the brain that control other addictive behaviors like drug and alcohol abuse and nicotine addiction,” Zhiping Pang, assistant professor and senior author, said in a press release.
A drug that mimics GLP-1 to improve glucose tolerance is currently available and has been recently approved as treatment for obesity, but it has significant side effects.
As research on how the central nervous system regulates food consumption behavior continues to progress, our understanding of the neural mechanisms that drive overeating and obesity are likely to expand.
