Ghrelin is a peptide predominantly produced by the stomach, although expressed by many other tissues, including the pancreas and the cardiovascular system. Its secretion is negatively associated to body mass index and undergoes fluctuations during the day. It is stimulated by energy restriction and acetylcholine, while it is reduced by gastrectomy, food intake, glucose, insulin and SRIF. Ghrelin is a natural ligand of the GH secretagogue (GHS) receptor 1a (GHS-R1a), known being specific for synthetic GHS. GHS-R1a expression and binding studies showed GHS-R in the hypothalamus-pituitary area but also in other brain areas as well as in peripheral, endocrine and non-endocrine tissues, including the pancreas and the cardiovascular system. Besides its potent GH-releasing effect, ghrelin: 1) stimulates lactotroph and corticotroph secretion while it negatively modulates the gonadal axis; 2) exerts central actions including orexigenic effect coupled with control of energy expenditure; 3) influences either the exocrine or the endocrine pancreatic function and the glucose and lipid metabolism; 4) controls gastric motility and acid secretion; 5) exerts cardiovascular actions; 6) modulates cell proliferation. Ser3-acylation of ghrelin is essential for binding the GHS-R1a and for its endocrine actions. However, both non-acylated and acylated ghrelin are bound by GHS-R subtypes at both the pancreatic and the cardiovascular level. Non-acylated ghrelin is not an inactive peptide; it exerts some non-endocrine actions such as cardiovascular activities, modulation of cell proliferation and even some metabolic action such as modulation of insulin secretion, glucose and lipid metabolism. Notably, some GHS-R subtypes are not ghrelin receptors; cardiovascular receptors specific for peptidyl GHS have been found and it has been shown they mediate some specific actions that are not shared by ghrelin.
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