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Ghrelin is a hormone that was believed to accumulate during periods of fasting and is found in the body in high concentrations just before meals.
It is dubbed the ‘hunger hormone’ because it has been shown that administration of therapeutic doses acts in the brain to stimulate hunger and increase food intake in animal models and humans.
A new lab study turns the current model about ghrelin (hunger hormone) on its head and point to a novel stomach enzyme (GOAT) responsible for the ghrelin activation that could be targeted in metabolic diseases.
Ghrelin requires the addition of a fatty acid by a specific enzyme (ghrelin O-acyl transferase, or GOAT) for activation. Previously, it was assumed that the fatty acids attached to ghrelin by GOAT were produced by the body during fasting.
New data unearthed by Matthias Tschop, a University of Cincinnati (UC) associate professor of internal medicine, and his team suggests that such fatty acids required for ghrelin activation come directly from ingested dietary fats.
In a departure from an earlier decade-long model, Tschop says, the ghrelin system seems to be 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.
Tschop and his team used mouse models to test the effects of over expressing the GOAT enzyme. They found that, 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, said an UC release.
‘When exposed to certain fatty foods, mice with more GOAT gain more fat,’ says Tschop. ‘Mice without GOAT gain less fat since their brain does not receive the ‘fats are here, store them’ signal.’
Other studies showed that during fasting, active ghrelin levels were flat, but during the presence of fat from foods, ghrelin levels peaked with meals.
Tschop says these human studies support the new model for ghrelin.
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