ArticleDiabetes2013
In situ electrophysiological examination of pancreatic α cells in the streptozotocin-induced diabetes model, revealing the cellular basis of glucagon hypersecretion.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Intra-Islet Paracrine Regulation of Glucagon Secretion During Hypoglycemia, Euglycemia, and Hyperglycemia.Annals of the New York Academy of Sciences · 2026Review
- Pancreatic α-cells are functionally heterogeneous and sex-dependently regulated by neighboring endocrine cells.Communications biology · 2026Article
- β-Cell Obligation in α-Cell Glucagon Response to Low Glucose.Research square · 2026Article
- The crucial role of potassium ion channels in diabetes mellitus and its complications: A review.Channels (Austin, Tex.) · 2025Review
- Efficient transduction of pancreas tissue slices with genetically encoded calcium integrators.bioRxiv : the preprint server for biology · 2025Article
- Calcium Imaging and Analysis in Beta Cells in Acute Mouse Pancreas Tissue Slices.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Bridging the Gap: Pancreas Tissue Slices From Organ and Tissue Donors for the Study of Diabetes Pathogenesis.Diabetes · 2024Review
- Article
- α-cell electrophysiology and the regulation of glucagon secretion.The Journal of endocrinology · 2023Review
- Misrouting of glucagon and stathmin-2 towards lysosomal system of α-cells in glucagon hypersecretion of diabetes.Islets · 2022Article
- Review
- Article
- In Vitro Disease Models of the Endocrine Pancreas.Biomedicines · 2021Review
- Glucokinase intrinsically regulates glucose sensing and glucagon secretion in pancreatic alpha cells.Scientific reports · 2020Article
- A 3D atlas of the dynamic and regional variation of pancreatic innervation in diabetes.Science advances · 2020Article
- Cell Heterogeneity and Paracrine Interactions in Human Islet Function: A Perspective Focused in β-Cell Regeneration Strategies.Frontiers in endocrinology · 2020Review
- Pancreatic alpha-cell mass in the early-onset and advanced stage of a mouse model of experimental autoimmune diabetes.Scientific reports · 2019Article
- Plasticity in the Glucagon Interactome Reveals Novel Proteins That Regulate Glucagon Secretion in α-TC1-6 Cells.Frontiers in endocrinology · 2018Article
- Human beta cell mass and function in diabetes: Recent advances in knowledge and technologies to understand disease pathogenesis.Molecular metabolism · 2017Review
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
Abstract
Early-stage type 1 diabetes (T1D) exhibits hyperglucagonemia by undefined cellular mechanisms. Here we characterized α-cell voltage-gated ion channels in a streptozotocin (STZ)-induced diabetes model that lead to increased glucagon secretion mimicking T1D. GYY mice expressing enhanced yellow fluorescence protein in α cells were used to identify α cells within pancreas slices. Mice treated with low-dose STZ exhibited hyperglucagonemia, hyperglycemia, and glucose intolerance, with 71% reduction of β-cell mass. Although α-cell mass of STZ-treated mice remained unchanged, total pancreatic glucagon content was elevated, coinciding with increase in size of glucagon granules. Pancreas tissue slices enabled in situ examination of α-cell electrophysiology. α cells of STZ-treated mice exhibited the following: 1) increased exocytosis (serial depolarization-induced capacitance), 2) enhanced voltage-gated Na(+) current density, 3) reduced voltage-gated K(+) current density, and 4) increased action potential (AP) amplitude and firing frequency. Hyperglucagonemia in STZ-induced diabetes is thus likely due to increased glucagon content arising from enlarged glucagon granules and increased AP firing frequency and amplitude coinciding with enhanced Na(+) and reduced K(+) currents. These alterations may prime α cells in STZ-treated mice for more glucagon release per cell in response to low glucose stimulation. Thus, our study provides the first insight that STZ treatment sensitizes release mechanisms of α cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.