Abstract
Ghrelin, a 28-amino acid peptide hormone expressed in X/A-like endocrine cells of the stomach, is the only known peripherally produced and centrally acting peptide that stimulates food intake and therefore attracted a lot of attention with one major focus on the treatment of conditions where an increased energy intake or body weight gain is desired. Anorexia nervosa is an eating disorder characterized by a pronounced reduction of body weight, a disturbed body image and hormonal alterations. Ghrelin signaling has been thoroughly investigated under conditions of anorexia nervosa. The present review will highlight these alterations of ghrelin in anorexia and discuss possible treatment strategies targeting ghrelin signaling. Lastly, gaps in knowledge will be mentioned to foster future research.
Highlights
Ghrelin was discovered in 1999 by Kojima and colleagues as an endogenous ligand of the growth hormone secretagogues receptor 1a (GHSR1a) stimulating the release of growth hormone (GH) from the pituitary [1] leading to the release of insulin-like growth factor 1 (IGF-1) [2]
Acylated ghrelin is able to bind to and activate the GHSR1a leading to, among other effects, a stimulation of food intake [8], reduction of insulin secretion resulting in hyperglycemia [9] and stimulation of gastric motility [10], whereas desacyl ghrelin—long thought to represent a non-active form of ghrelin—is assumed to counterbalance the orexigenic effect of acyl ghrelin [11,12]
Following up on these findings in studies comparing anorexia nervosa (AN) to normal weight controls, in 2003 a study compared AN patients with body mass index (BMI)-matched healthy subjects showing that AN patients had doubled fasting and 24-h plasma ghrelin levels compared to constitutionally lean subjects [70], giving rise to a role of ghrelin in the development or maintenance of AN
Summary
Ghrelin was discovered in 1999 by Kojima and colleagues as an endogenous ligand of the growth hormone secretagogues receptor 1a (GHSR1a) stimulating the release of growth hormone (GH) from the pituitary [1] leading to the release of insulin-like growth factor 1 (IGF-1) [2]. Ghrelin was found to be secreted from oxyntic glands in the gastric fundus [1] and the subsequent description of ghrelin’s effects on food intake, glucose metabolism and body weight followed soon thereafter [4]. Ghrelin is derived from preproghrelin and activated by acylation, namely by the attachment of a fatty acid side chain to its serine 3 residue catalyzed by the ghrelin-O-acyl transferase (GOAT) [5] Another peptide hormone is derived from this precursor, namely obestatin [6]. Acylated ghrelin is able to bind to and activate the GHSR1a leading to, among other effects, a stimulation of food intake [8], reduction of insulin secretion resulting in hyperglycemia [9] and stimulation of gastric motility [10], whereas desacyl ghrelin—long thought to represent a non-active form of ghrelin—is assumed to counterbalance the orexigenic effect of acyl ghrelin [11,12]. Gaps in knowledge will be addressed to stimulate future research
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