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Minireview: Glucagon in the Pathogenesis of Hypoglycemia and Hyperglycemia in Diabetes
Open accessAbstract
Pancreatic islet α-cell glucagon secretion is critically dependent on pancreatic islet β-cell insulin secretion. Normally, a decrease in the plasma glucose concentration causes a decrease in β-cell insulin secretion that signals an increase in α-cell glucagon secretion during hypoglycemia. In contrast, an increase in the plasma glucose concentration, among other stimuli, causes an increase in β-cell insulin secretion that signals a decrease, or at least no change, in α-cell glucagon secretion after a meal. In absolute endogenous insulin deficiency (i.e. in type 1 diabetes and in advanced type 2 diabetes), however, β-cell failure results in no decrease in β-cell insulin secretion and thus no increase in α-cell glucagon secretion during hypoglycemia and no increase in β-cell insulin secretion and thus an increase in α-cell glucagon secretion after a meal. In type 1 diabetes and advanced type 2 diabetes, the absence of an increment in glucagon secretion, in the setting of an absent decrement in insulin secretion and an attenuated increment in sympathoadrenal activity, in response to falling plasma glucose concentrations plays a key role in the pathogenesis of iatrogenic hypoglycemia. In addition, there is increasing evidence that, in the aggregate, suggests that relative hyperglucagonemia, in the setting of deficient insulin secretion, plays a role in the pathogenesis of hyperglycemia in diabetes. If so, abnormal glucagon secretion is involved in the pathogenesis of both hypoglycemia and hyperglycemia in diabetes.
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In the citing paper
“Besides insulin, glucagon is a major hormone in glucose homeostasis and plays a role in the pathogenesis of hyperglycaemia in diabetes (as reviewed by Cryer PE [35]).”
From Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats (2015) · cites this paper as [35]
In the citing paper
“Furthermore, there is a paradoxical impairment of glucagon secretion during hypoglycemia in patients with diabetes.”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [25]
In the citing paper
“The relative insulin excess increases glucose uptake and suppresses glucose production in the liver, despite the development of hypoglycemia.”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [25]
In the citing paper
“In individuals with T1D or prolonged type 2 diabetes (T2D), unregulated insulin release from subcutaneous depots or the sustained effects of sulfonylureas can result in elevated systemic insulin levels during hypoglycemia.”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [25]
In the citing paper
“Hormonal dysregulation has been identified as a significant factor contributing to the development of hypoglycemia unawareness syndrome.”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [25]
In the citing paper
“In addition, beta-cell dysregulation leads to dysfunction of alpha-cells, and a lack of a decrease in insulin levels prevents glucagon secretion.”
From Hypoglycemia Unawareness—A Review on Pathophysiology and Clinical Implications (2024) · cites this paper as [25]
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Dysregulated plasma glucagon levels in Japanese young adult type 1 diabetes patients
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Metadata
- Authors
- Cryer, P. E.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Cryer, Philip E.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2012-03-01
- Volume
- 153
- Issue
- 3
- Pages
- 1039-1048
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC3281526
- OpenAlex
- W2041654060
- Cited by
- 242
- References
- 117
- Citations by year
- 2026: 6 · 2025: 15 · 2024: 14 · 2023: 16 · 2022: 15 · 2021: 28 · 2020: 11 · 2019: 16 · 2018: 17 · 2017: 17 · 2016: 15 · 2015: 14 · 2014: 23 · 2013: 27 · 2012: 8
- FWCI
- 3.27
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrinology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p60dk020579-35)
- National Institute of Diabetes and Digestive and Kidney Diseases (R37DK027085, P60-DK20579, P60-DK-020579, P30DK020579, T32DK007120)
- National Center for Research Resources (UL1RR024992, M01RR000036)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- glucagon secretion, beta-cell insulin secretion, hypoglycemia, hyperglycemia, type 1 diabetes, type 2 diabetes, iatrogenic hypoglycemia, hyperglucagonemia, beta-cell failure, sympathoadrenal activity, glucose homeostasis
- MeSH terms
- Animals, Diabetes Mellitus, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Glucagon, Humans, Hyperglycemia, Hypoglycemia, Insulin, Models, Biological, Somatostatin, Glucagon-Secreting Cells, Mice, Rats
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