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Minireview: Glucagon in the Pathogenesis of Hypoglycemia and Hyperglycemia in Diabetes

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Cryer, Philip E.·2012·Endocrinology

DOI 10.1210/en.2011-1499PMC PMC3281526

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Abstract

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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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
DOI: 10.1210/en.2011-1499
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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Minireview: Glucagon in the Pathogenesis of Hypoglycemia and Hyperglycemia in Diabetes

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