Islet cell function: α and β cells - partners towards normoglycaemia: α and β cells and normoglycaemia
Open accessAbstract
Under normal conditions, insulin and glucagon are counter-regulatory hormones whose balanced action exhibits a relationship that ensures normoglycaemia. Elevated glucose levels following a meal stimulate pancreatic islet beta cells to secrete insulin and islet alpha cells to downregulate production of glucagon. With declining glucose and insulin levels, alpha-cell production of glucagon is increased to stimulate hepatic glucose production, preventing fasting hypoglycaemia. In type 2 diabetes mellitus (T2DM), beta-cell insulin response to glucose is blunted, including absence of early acute response, and alpha-cell response to glucose is impaired, resulting in absolute or relative hyperglucagonaemia and inappropriate hepatic glucose output that contributes to fasting hyperglycaemia. These changes are associated with structural and functional changes in pancreatic islets, including reduced beta-cell mass and reduced beta-cell:alpha-cell ratio. The role of the incretin hormone glucagon-like peptide-1 (GLP-1) in regulating glucose-dependent beta-cell insulin production and glucose-dependent alpha-cell glucagon production has been used to develop GLP-1-based therapies. These therapies may reduce the imbalances among insulin and glucagon that characterise T2DM, resulting in improved glycaemic control.
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Glucagon increases blood glucose levels.
“Glucagon increases blood glucose levels, whereas insulin decreases them.5”
From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [5]
Insulin decreases blood glucose levels.
“Glucagon increases blood glucose levels, whereas insulin decreases them.5”
From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [5]
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- Authors
- Göke, B.
- Affiliations
- Ludwig-Maximilians-Universität München (DE)
- Corresponding author
- Göke, B.
- Venue
- International Journal of Clinical Practice
- Publisher
- Wiley
- Published
- 2008-02-05
- Volume
- 62
- Issue
- 159
- Pages
- 2-7
- ISSN
- 1368-5031 (ISSN-L)
- OpenAlex
- W1506458831
- Cited by
- 58
- References
- 21
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 5 · 2022: 2 · 2021: 6 · 2020: 4 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 5 · 2015: 2 · 2014: 2 · 2013: 6 · 2012: 1
- FWCI
- 3.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Clinical Practice (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Novartis Pharma
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- pancreatic islet cells, alpha cells, pancreatic beta cells, insulin, glucagon, normoglycemia, type 2 diabetes, hyperglucagonaemia, hepatic glucose production, fasting hyperglycemia, beta-cell mass, glucagon-like peptide-1, GLP-1 receptor agonists, incretins, glucose-dependent insulin secretion
- MeSH terms
- Animals, Diabetes Mellitus, Glucagon, Glucose, Humans, Insulin, Islets of Langerhans, Postprandial Period, Glucagon-Secreting Cells, Insulin-Secreting Cells, Glucagon-Like Peptide 1
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