Fatty Foods Stimulate Hunger
It's Not an Empty Stomach That Stimulates
The Hunger Hormone... It's Fatty Foods!
The Hunger Hormone... It's Fatty Foods!
New research led by the University of Cincinnati (UC) suggests that the hunger hormone called Ghrelin is activated by fats from the foods we eat, not those made in the body, in order to optimize nutrient metabolism and promote the storage of body fat.
The new findings turn the current model about Ghrelin in a different direction and point to a specific stomach enzyme (G.O.A.T) responsible for the "ghrelin"activation process that could be targeted in future treatments for metabolic diseases. The laboratory study is published online in the Journal Nature Medicine.
Ghrelin is a hormone which was believed to accumulate during periods of fasting and is found in the body in high concentrations just before meals. It is also known as the "hunger hormone" because it has been shown that administration of pharmacological doses acts in the brain to stimulate hunger and increase food intake in animal models and humans.
The Ghrelin hormone is unique in that it requires the addition of a fatty acid
(acylation)by a specific enzyme called Ghrelin O-Acyl Transferase (G.O.A.T) for activation. Originally, it was assumed that the fatty acids attached to Ghrelin by G.O.A.T were produced by the body during fasting.
The new data suggests that the fatty acids needed for Ghrelin activation
actually come directly from ingested dietary fats. In a departure from an earlier model that was upheld for nearly a decade, 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.
The research team tested the effects on subjects by over expressing the G.O.A.T enzyme, or knocking it out. They found that, when exposed to a lipid-rich diet, subjects without GOAT accumulated less fat than normal subjects, while those with over-expressed G.O.A.T accumulated more fat mass than normal subjects.
The researchers demonstrated that when exposed to certain fatty foods, subjects with more G.O.A.T gain more fat. Conversely, the subjects without G.O.A.T gain less fat since their brain does not receive the "fats are here, store them" signal.
Recent human studies at the University of Virginia measured (separately) active and inactive Ghrelin concentrations. Those studies showed that during fasting, active Ghrelin levels were flat, but during the presence of fat from foods, Ghrelin levels peaked with meals as previously described. These human studies support the new model for Ghrelin hormone activity.
The researchers are particularly interested in how Ghrelin may be involved in the rapid benefits of gastric bypass surgery, the obesity therapy which frequently reduces appetite and improves metabolism before substantial weight loss occurs. Intriguingly, this procedure causes food to bypass the stomach and gut sections that contain G.O.A.T/Ghrelin cells, which, based on this newly described model, would prevent Ghrelin activation.
The study was supported by the Leibniz Graduate College and by the
National Institutes of Health's National Institute of Diabetes and Digestive
and Kidney Diseases.
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