Surely we become hungry because our stomach is empty, right? This has long been the point of research surrounding the "hunger hormone" ghrelin. We've had opportunity to discuss ghrelin on many previous occasions, as it is believed to be key to hunger management and therefore weight loss. But recent research is demonstrating that ghrelin may operate very differently than previously believed—and that it may be the presence of fatty foods that triggers ghrelin's activity.
Only discovered about a decade ago, ghrelin has been shown to have a major role in regulating hunger. And yet, the hormone is still only beginning to be understood. Until now, researchers have believed that ghrelin builds up whenever we don't eat, becoming particularly concentrated just before meals, and potentially causing us to overeat if we delay meals and allow it to build up too far.
New research seems to indicate, however, that ghrelin may work very differently—and that, in fact, it is the fat in foods that gives ghrelin its punch. That's because ghrelin requires the addition of fatty acids to become active. Until now, researchers have believed that those fatty acids were produced internally during fasting. Now, researchers at the University of Cincinnati have found that the fatty acids come from our food and are bound to the ghrelin by an enzyme. The study, published in the journal Nature, found that mice high in the binding enzyme and given a fatty diet gain more fat, whereas mice low in the enzyme gain less fat. The meeting of enzyme and ghrelin doesn't just trigger hunger—it triggers weight gain as well. Why?
It is important to remember that, while many of us suffer from an excess of calories in our lives, this is a recent phenomenon in the history of our evolution. We are actually designed to suck as many calories as possible from our food, and turn as much of those as possible to fat. So, ghrelin, once triggered by the presence of fatty food, tells the calorie-maximizing systems in the body —the ones responsible for growth and fat storage—that the stomach is holding calories ready for absorption. As lead researcher Dr. Matthias Tschöp says, the low-enzyme mice gain less weight because "their brain does not receive the 'fats are present' signal."
As Dr. Tschöp points out, this may help explain the success of gastric bypass surgeries: "This powerful obesity therapy frequently reduces appetite and improves metabolism before substantial weight loss occurs," he says. "Intriguingly, this procedure causes food to bypass the stomach and gut sections that contain... ghrelin cells, which, based on this newly described model, would prevent ghrelin activation.” For dieters, this research offers hope for a means to block the meeting of enzyme and ghrelin, and thus to break the familiar cycle whereby a rich meal rapidly triggers hunger for another such meal.