The role of ghrelin in the regulation of glucose homeostasis
Open accessAbstract
Ghrelin is a 28-amino acid (aa) stomach-derived peptide discovered in 1999 as the endogenous ligand for growth hormone secretagogue-receptor (GHS-R). Ghrelin-producing cells constitute a distinct group of endocrine cells dispersed throughout the gastric mucosa and to a lesser extent in the small intestine and the endocrine pancreas. Ghrelin plasma levels rise during fasting and chronic caloric restriction to stimulate food intake and fat storage and to prevent life-threatening falls in blood glucose. Plasma ghrelin levels decrease after a meal is consumed and in conditions of energy surplus (such as obesity). Ghrelin has emerged as a key player in the regulation of appetite and energy homeostasis. Ghrelin achieves these functions through binding the ghrelin receptor GHS-R in appetite-regulating neurons and in peripheral metabolic organs including the endocrine pancreas. Ghrelin levels are negatively correlated with body mass index (BMI) and insulin resistance. In addition, ghrelin secretion is impaired in obesity and insulin resistance. Several studies highlight an important role for ghrelin in glucose homeostasis. Genetic, immunological, and pharmacological blockade of ghrelin signaling resulted in improved glucose tolerance and insulin sensitivity. Furthermore, exogenous ghrelin administration was shown to decrease glucose-induced insulin release and increase glucose level in both humans and rodents. GHS-R was shown to be expressed in pancreatic β-cells and ghrelin suppressed insulin release via a Ca2+-mediated pathway. In this review, we provide a detailed summary of recent advances in the field that focuses on the role of insulin and insulin resistance in the regulation of ghrelin secretion and on the role of ghrelin in glucose-stimulated insulin secretion (GSIS).
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The postprandial decrease in ghrelin lowers hepatic glucose production while increasing peripheral glucose-uptake in both skeletal muscle and adipose tissue.
“The postprandial decrease in ghrelin lowers hepatic glucose production while increasing peripheral glucose-uptake in both skeletal muscle and adipose tissue (113).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [113]
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- Authors
- Alamri, B. N., Shin, K., Chappe, V., & Anini, Y.
- Affiliations
- Dalhousie University (CA)
- Venue
- Hormone Molecular Biology and Clinical Investigation
- Publisher
- Walter de Gruyter GmbH
- Published
- 2016-04-01
- Volume
- 26
- Issue
- 1
- Pages
- 3-11
- ISSN
- 1868-1883 (ISSN-L)
- 1868-1891
- OpenAlex
- W2411901770
- Cited by
- 93
- References
- 59
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 6 · 2023: 14 · 2022: 13 · 2021: 14 · 2020: 7 · 2019: 12 · 2018: 7 · 2017: 9 · 2016: 1
- FWCI
- 1.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hormone Molecular Biology and Clinical Investigation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (MOP-82795)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- ghrelin, glucose homeostasis, growth hormone secretagogue receptor, insulin resistance, glucose-stimulated insulin secretion, pancreatic beta cells, insulin secretion, ghrelin secretion, obesity, energy homeostasis, appetite regulation, calcium signaling
- MeSH terms
- Animals, Blood Glucose, Homeostasis, Humans, Insulin, Signal Transduction, Ghrelin
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