Hunger may not stem from an empty stomach, but rather from fats of the foods we eat. This turns the current model about hunger hormone ghrelin on its head, the study’s author says.
Matthias Tschöp, MD, associate professor of psychiatry and internal medicine,
University of Cincinnati, authored the study published in the current issue of
Nature Medicine.
Ghrelin, called the “hunger hormone,” was long-believed to accumulate during fasting periods and before meals. Prior animal and human trials found that ghrelin stimulated hunger and increased food intake.
The hunger hormone, however, needs the assistance of the fatty acid GOAT (ghrelin O-acyl transferase) to activate. Once activated, ghrelin optimizes nutrient metabolism and promotes the storage of body fat.
Activating the hunger hormone
For nearly a decade, it has been assumed that the fatty acids attached to ghrelin by GOAT were produced by the body during fasting. Tschöp and team found this not to be the case. Instead, the needed fatty acids originated from ingested dietary fats.
It appears that the ghrelin system is a lipid sensor in the stomach that informs the brain when calories are available—giving the green light to other calorie-consuming processes such as growing.
In the study, mice with and without GOAT were used. “When exposed to a lipid-rich diet, mice without GOAT accumulated less fat than normal mice, while those with over-expressed GOAT accumulated more fat mass than normal mice.”
Implications in humans
Recently, human studies at the University of Virginia discovered that during fasting, active ghrelin levels were flat, but during the presence of fat from foods, ghrelin levels peaked with meals.
Tschöp is currently looking into how ghrelin is involved after gastric bypass surgery. Meanwhile, the stomach enzyme GOAT may be used to develop treatments for metabolic diseases.
