Las comidas grasas activan la hormona del hambre/ Fatty foods fire up hunger hormone

Investigaciones lideradas por la Universidad de Cincinnati (UC - E.E.U.U.) sugieren que la hormona del hambre, ghrelin o grelina, es activada por las grasas que comemos, y no por las que están ya en el cuerpo, para optimizar el metabolismo de los nutrientes y promover el amacenamiento de grasa corporal.
Este hallazgo, según Matthias Tschöp (UC) ponen del revés el actual modelo de ghrelin, y apuntan a una nueva enzima estomacal (GOAT) como responsable del proceso de activación de la ghrelin, y la convierte en objetivo de los futuros tratamientos de trastornos metabólicos.
La ghrelin es una hormona que se pensaba se acumulaba durante los períodos de ayuno y que se encuentra en el organismo en elevadas concentraciones justo antes de las comidas. Se la llama "la hormona del hambre" porque se ha demostrado que su administración en dosis farmacológicas, actúa sobre el cerebro para estimular el apetito y aumentar la ingesta de alimentos en animales y humanos.
La ghrelin precisa de su acilación (adicición de un ácido graso) por una hormona específica (ghrelin O-acil transferase, GOAT) para ser activada. Antes se suponía que los ácidos grasos que se unían a la ghrelin eran producidos por el organismo durante el ayuno, pero los nuevos datos de Tschöp y su equipo, sugieren que los ácidos grasos necesarios para activar la ghrelin vienen en realidad directamente de las grasas ingeridas en la dieta. Parece que la ghrelin es una especie de sensor estomacal de grasas que informa al cerebro de que hay calorías disponibles.
Los periodos de ayuno, por lo tanto, no aumentarían los niveles de grelina, lo que puede dar un nuevo enfoque al tratamiento de la obesidad.
El artículo ha aparecido on-line en la revista Nature (5 de junio)

A research led by the University of Cincinnati (UC - USA) suggests that the hunger hormone 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 findings, according to Matthias Tschöp (UC), turn the current model about ghrelin on its head and point to a novel stomach enzyme (GOAT) responsible for the ghrelin activation process that could be targeted in future treatments for metabolic diseases.
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 pharmacological doses acts in the brain to stimulate hunger and increase food intake in animal models and humans.
The ghrelin hormone requires acylation (the addition of a fatty acid) by a specific enzyme (ghrelin O-acyl transferase, or GOAT) for activation. Originally it was assumed that the fatty acids attached to ghrelin by GOAT were produced by the body during fasting, but the new data by Tschöp and his team suggests that the fatty acids needed for ghrelin activation actually come directly 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.
Therefore, fasting periods, do not increase the levels of ghrelin, and this fact could can give a new approach to the treatment of the obesity.
The paper is published online on June 5, 2009, in the journal Nature Medicine.

Tomado de/ Taken from University of Cincinnati

Resumen de la publicación/ Abstract of the paper
GOAT links dietary lipids with the endocrine control of energy balance
Henriette Kirchner, Jesus A Gutierrez, Patricia J Solenberg, Paul T Pfluger, Traci A Czyzyk, Jill A Willency, Annette Schürmann, Hans-Georg Joost, Ronald J Jandacek, John E Hale, Mark L Heiman and Matthias H Tschöp , Nature Medicine Published online: 5 June 2009 doi:10.1038/nm.1997
Central nervous system nutrient sensing and afferent endocrine signaling have been established as parallel systems communicating metabolic status and energy availability in vertebrates. The only afferent endocrine signal known to require modification with a fatty acid side chain is the orexigenic hormone ghrelin. We find that the ghrelin O-acyl transferase (GOAT), which is essential for ghrelin acylation, is regulated by nutrient availability, depends on specific dietary lipids as acylation substrates and links ingested lipids to energy expenditure and body fat mass. These data implicate the ghrelin-GOAT system as a signaling pathway that alerts the central nervous system to the presence of dietary calories, rather than to their absence as is commonly accepted.