@article{TGC4853,
author = {Weiyi Chen and Pablo J. Enriori},
title = {Ghrelin: a journey from GH secretagogue to regulator of metabolism},
journal = {Translational Gastrointestinal Cancer},
volume = {4},
number = {1},
year = {2014},
keywords = {},
abstract = {Over the past two decades, ghrelin has evolved from a growth hormone secretagogue to an essential metabolic regulator of energy and glucose homeostasis. Obesity is associated with significant disturbances in metabolic function and its prominence as a global health issue is gaining momentum. The rising rates of mortality in relation to metabolic dysfunctions necessitate the discovery of new therapeutics to combat obesity and diabetes. Here in this review, we discuss the relevant information relating to ghrelin, its receptor and how ghrelin regulates energy metabolism through brain centers and peripheral organs. Ghrelin has a unique structure with a n-octanoyl ester at its third serine residue, which serves as an endogenous ligand to growth hormone secretagogue receptor (GHS-1Ra). Upon activation of orexigenic NPY/AgRP neurons by ghrelin, anorexigenic proopiomelanocortin (POMC) neurons are concurrently suppressed through the inhibitory γ-aminobutyric acid (GABA)-eric inputs from activated NPY/AgRP neurons to regulate food intake. Due to its orexigenic nature, ghrelin may have a beneficial effect on restoring neutral energy balance in catabolic conditions such as cancer cachexia and age-related frailty. However, emerging studies have unveiled the paramount role of ghrelin on peripheral organs such as the pancreas, liver, skeletal muscles and adipocytes to regulate glucose homeostasis. Collectively, this review highlights the potential targets of ghrelin as a metabolic regulator; and briefly discusses the role of ghrelin in relation to gastrointestinal cancers. This knowledge may aid in the development of future therapeutic strategies to battle not just metabolic diseases but also weight loss in cancer and age-related conditions.},
url = {https://tgc.amegroups.com/article/view/4853}
}