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Overeating? It May Be All in Your Head
Eat when you feel hungry, Stop when you don’t. But what if you never feel full?
With the ongoing obesity epidemic in America, a new study from Johns Hopkins that provides a deeper understanding of satiety — the sensation of fullness and satisfaction after eating — could help point the way to new treatments for people prone to overeating.
While investigating the brain’s memory and learning systems in mice, scientists came across a particular type of brain cell that sends signals to the body that when it comes to that extra helping, enough is enough.
“When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after,” says Richard Huganir, Ph.D., director of the Department of Neuroscience at the Johns Hopkins University School of Medicine. “The signals seem to tell the mice they’ve had enough.”
A Surprising On/Off Switch for Appetite
In examining these signals between nerve cells in the brain, Huganir, along with graduate student Olof Lagerlöf, M.D., and other colleagues, focused on a particular enzyme called OGT that is involved in how the body uses sugar and insulin. When they deleted the enzyme from the brains of mice, it effectively removed the “off switch” to the animals’ appetites, and those mice began to eat bigger meals and gain weight, mostly in the form of body fat.
Getting the Message You’ve Had Enough to Eat
With the mice now supersizing their portions at every turn, the researchers wondered, were the brains of the mice not getting the message that they had had enough to eat?
To test the theory, the researchers used light to stimulate these specific brain cells. With the lines of communication now open, the formerly overeating mice decreased their food consumption by 25 percent.
Glucose, the simple sugar that rises in the bloodstream after eating, plays a role in how the brain enzyme works. After a meal, when the system is working normally, it’s possible that a derivative of glucose helps OGT do its job and activate the “I’m full” appetite shut-off mechanism.
“We believe we have found a new receiver of information that directly affects brain activity and feeding behavior, and if our findings bear out in other animals, including people, they may advance the search for drugs or other means of controlling appetites,” says Lagerlöf.