Unraveling the role of the ghrelin gene peptides in the endocrine pancreas
Abstract
The ghrelin gene peptides include acylated ghrelin (AG), unacylated ghrelin (UAG), and obestatin (Ob). AG, mainly produced by the stomach, exerts its central and peripheral effects through the GH secretagogue receptor type 1a (GHS-R1a). UAG, although devoid of GHS-R1a-binding affinity, is an active peptide, sharing with AG many effects through an unknown receptor. Ob was discovered as the G-protein-coupled receptor 39 (GPR39) ligand; however, its physiological actions remain unclear. The endocrine pancreas is necessary for glucose homeostasis maintenance. AG, UAG, and Ob are expressed in both human and rodent pancreatic islets from fetal to adult life, and the pancreas is the major source of ghrelin in the perinatal period. GHS-R1a and GPR39 expression has been shown in β-cells and islets, as well as specific binding sites for AG, UAG, and Ob. Ghrelin colocalizes with glucagon in α-islet cells, but is also uniquely expressed in ε-islet cells, suggesting a role in islet function and development. Indeed, AG, UAG, and Ob regulate insulin secretion in β-cells and isolated islets, promote β-cell proliferation and survival, inhibit β-cell and human islet cell apoptosis, and modulate the expression of genes that are essential in pancreatic islet cell biology. They even induce β-cell regeneration and prevent diabetes in streptozotocin-treated neonatal rats. The receptor(s) mediating their effects are not fully characterized, and a signaling crosstalk has been suggested. The present review summarizes the newest findings on AG, UAG, and Ob expression in pancreatic islets and the role of these peptides on β-cell development, survival, and function.
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Ghrelin stimulates hunger and food intake, reduces energy expenditure, and promotes fat retention.
“In contrast to leptin, ghrelin stimulates hunger and food intake, reduces EE, and promotes the retention of fat [56, 58, 92, 191].”
From Sleep and metabolic function (2012) · cites this paper as [58]
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“In contrast to leptin, ghrelin stimulates hunger and food intake, reduces EE, and promotes the retention of fat [56, 58, 92, 191].”
Spiegel, K., Tasali, E., Leproult, R., Scherberg, N., & Van Cauter, E. (2011) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2010-1978 · Cited by 106 · see citing works
- Authors
- Granata, R., Baragli, A., Settanni, F., Scarlatti, F., & Ghigo, E.
- Affiliations
- University of Turin (IT)
- Venue
- Journal of Molecular Endocrinology
- Publisher
- Bioscientifica
- Published
- 2010-07-01
- Volume
- 45
- Issue
- 3
- Pages
- 107-118
- ISSN
- 0952-5041 (ISSN-L)
- 1479-6813
- OpenAlex
- W2123429118
- Cited by
- 97
- References
- 90
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 5 · 2018: 3 · 2017: 7 · 2016: 6 · 2015: 3 · 2014: 8 · 2013: 20 · 2012: 12
- FWCI
- 17.19
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- ghrelin, acylated ghrelin, unacylated ghrelin, obestatin, endocrine pancreas, pancreatic islets, pancreatic beta cells, beta-cell proliferation, beta-cell apoptosis, insulin secretion, GHS-R1a, GPR39, glucagon, beta cell regeneration, glucose homeostasis, diabetes prevention
- MeSH terms
- Insulin Secretion, Acylation, Animals, Cell Survival, Humans, Insulin, Islets of Langerhans, Insulin-Secreting Cells, Ghrelin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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