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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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Marroquí, L., Vieira, E. C., González, A., Nadal, Á., & Quesada, I. (2011) · Diabetologia · doi:10.1007/s00125-010-2024-1 · Cited by 30
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The vascular order of islet cellular perfusion in the human pancreas
Stagner, J. I., & Samols, E. (1992) · Diabetes · doi:10.2337/diabetes.41.1.93 · Cited by 27
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Osei, K., O’Dorisio, T. M., Malarkey, W. B., Craig, E. L., & Cataland, S. (1989) · Diabetes · doi:10.2337/diab.38.6.704 · Cited by 21
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Basal insulin, glucagon, and growth hormone replacement
Breckenridge, S. M., Raju, B., Arbeláez, A. M., Patterson, B. W., Cooperberg, B. A., & Cryer, P. E. (2007) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00325.2007 · Cited by 7
Self-citationPartial Inhibition of Insulin Secretion Results in Glucose Intolerance but Not Hyperglucagonemia
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Self-citationDoes glucagon have a lipolytic effect?
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Flagged first, then by citations
1 of the 117 references couldn’t be matched to a known paper.
Research works printed but not linked: 4
- Samols, 1972, Glucagon-insulin interrelationships, 151
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Cited by
Sorted by citations
Physiology of Proglucagon Peptides: Role of Glucagon and GLP-1 in Health and Disease
Sandoval, D. A., & D'Alessio, D. A. (2015) · Physiological Reviews · doi:10.1152/physrev.00013.2014 · Cited by 498
Mechanisms of hypoglycemia-associated autonomic failure in diabetes
Cryer, P. E. (2013) · New England Journal of Medicine · doi:10.1056/nejmra1215228 · Cited by 433
Self-citationClassification, Pathophysiology, Diagnosis and Management of Diabetes Mellitus
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The Cells of the Islets of Langerhans
Xavier, G. D. S. (2018) · Journal of Clinical Medicine · doi:10.3390/jcm7030054 · Cited by 343
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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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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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