ArticleProceedings of the National Academy of Sciences of the United States of America2017
Glucagon receptor inhibition normalizes blood glucose in severe insulin-resistant mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 71 citations in OpenAlex.
- A first-in-human pharmacodynamic and pharmacokinetic study of a fully human anti-glucagon receptor monoclonal antibody in normal healthy volunteers.Diabetes, obesity & metabolism · 2018Trial
- Severe Insulin Resistance: Diagnosis and Management.Current diabetes reviews · 2026Review
- The neglected PCK1/glucagon (inter)action in nutrient homeostasis beyond gluconeogenesis: Disease pathogenesis and treatment.Molecular metabolism · 2025Review
- GLP-1 metabolite GLP-1(9-36) is a systemic inhibitor of mouse and human pancreatic islet glucagon secretion.Diabetologia · 2024Article
- The Regulation and Secretion of Glucagon in Response to Nutrient Composition: Unraveling Their Intricate Mechanisms.Nutrients · 2023Review
- α-cell electrophysiology and the regulation of glucagon secretion.The Journal of endocrinology · 2023Review
- PyCreas: a tool for quantification of localization and distribution of endocrine cell types in the islets of Langerhans.Frontiers in endocrinology · 2023Article
- Review
- Importance of multiple endocrine cell types in islet organoids for type 1 diabetes treatment.Translational research : the journal of laboratory and clinical medicine · 2022Review
- Sustained glucagon receptor antagonism in insulin-deficient high-fat-fed mice.The Journal of endocrinology · 2022Article
- Glucagon receptor signaling at white adipose tissue does not regulate lipolysis.American journal of physiology. Endocrinology and metabolism · 2022Article
- Review
- Insights into the Role of Glucagon Receptor Signaling in Metabolic Regulation from Pharmacological Inhibition and Tissue-Specific Knockout Models.Biomedicines · 2022Review
- Pro-α-cell-derived β-cells contribute to β-cell neogenesis induced by antagonistic glucagon receptor antibody in type 2 diabetic mice.iScience · 2022Article
- Acetyl-CoA-carboxylase 1 (ACC1) plays a critical role in glucagon secretion.Communications biology · 2022Article
- The mitochondrial β-oxidation enzyme HADHA restrains hepatic glucagon response by promoting β-hydroxybutyrate production.Nature communications · 2022Article
- Glucagon blockade restores functional β-cell mass in type 1 diabetic mice and enhances function of human islets.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Pathways of Glucagon Secretion and Trafficking in the Pancreatic Alpha Cell: Novel Pathways, Proteins, and Targets for Hyperglucagonemia.Frontiers in endocrinology · 2021Review
- Wild-Type Zebrafish (Animals : an open access journal from MDPI · 2020Review
- 3D quantification of changes in pancreatic islets in mouse models of diabetes type I and II.Disease models & mechanisms · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivating mutations in the insulin receptor results in extreme insulin resistance. The resulting hyperglycemia is very difficult to treat, and patients are at risk for early morbidity and mortality from complications of diabetes. We used the insulin receptor antagonist S961 to induce severe insulin resistance, hyperglycemia, and ketonemia in mice. Using this model, we show that glucagon receptor (GCGR) inhibition with a monoclonal antibody normalized blood glucose and β-hydroxybutyrate levels. Insulin receptor antagonism increased pancreatic β-cell mass threefold. Normalization of blood glucose levels with GCGR-blocking antibody unexpectedly doubled β-cell mass relative to that observed with S961 alone and 5.8-fold over control. GCGR antibody blockage expanded α-cell mass 5.7-fold, and S961 had no additional effects. Collectively, these data show that GCGR antibody inhibition represents a potential therapeutic option for treatment of patients with extreme insulin-resistance syndromes.
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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.