ReviewJournal of diabetes investigation2018
Regulation of amino acid metabolism and α-cell proliferation by glucagon.
Review in Journal of diabetes investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- The relationship between glucose and the liver-alpha cell axis - A systematic review.Frontiers in endocrinology · 2022Pooled it
- One Week Exposure to a Somatostatin Receptor 2 Antagonist (SSTR2a) Enhances Glucagon Counterregulation to Insulin-Induced Hypoglycaemia and Does Not Worsen Glycemia in a Male Rat Model of Insulin-Requiring Type 2 Diabetes.Diabetes, obesity & metabolism · 2026Article
- Inter-organ metabolic feedback via BCAA catabolism regulates glucagon-like hormone secretion in Drosophila.Nature communications · 2026Article
- Integrated Genomic-Metabolomic Analysis for Tri-Categorical Classification of Type 2 Diabetes Status in the Korean Ansan-Ansung Cohort.International journal of molecular sciences · 2025Article
- Article
- Clinical characteristics of Japanese Americans with normal glucose tolerance with 1-h hyperglycemia: A cross-sectional study.Journal of diabetes investigation · 2025Article
- Article
- Brain amino acid sensing for organismal amino acid homeostasis.Open biology · 2025Review
- Glucagon and Glucose Availability Influence Metabolic Heterogeneity and Malignancy in Pancreatic Neuroendocrine Tumour (pNET) Cells: Novel Routes for Therapeutic Targeting.Molecules (Basel, Switzerland) · 2025Article
- A Two-Hour Fetal Glucagon Infusion Stimulates Hepatic Catabolism of Amino Acids in Fetal Sheep.International journal of molecular sciences · 2025Article
- Liver-specific glucagon dysfunction promotes PP-cell hyperplasia and formation of glucagon and PP double-positive cells.PloS one · 2025Article
- Variable glucagon metabolic actions in diverse mouse models of obesity and type 2 diabetes.Molecular metabolism · 2024Article
- Phosphoproteomics-directed manipulation reveals SEC22B as a hepatocellular signaling node governing metabolic actions of glucagon.Nature communications · 2024Article
- Glucagon infusion alters the circulating metabolome and urine amino acid excretion in dogs.The Journal of endocrinology · 2024Article
- Advances in clinical research on glucagon.Diabetology international · 2024Review
- Advances in basic research on glucagon and alpha cells.Diabetology international · 2024Review
- Illuminating the complete ß-cell mass of the human pancreas- signifying a new view on the islets of Langerhans.Nature communications · 2024Article
- Blockade of glucagon increases muscle mass and alters fiber type composition in mice deficient in proglucagon-derived peptides.Journal of diabetes investigation · 2023Article
- Newly discovered knowledge pertaining to glucagon and its clinical applications.Journal of diabetes investigation · 2023Review
- A newly developed glucagon sandwich ELISA is useful for more accurate glucagon evaluation than the currently used sandwich ELISA in subjects with elevated plasma proglucagon-derived peptide levels.Journal of diabetes investigation · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both glucagon and glucagon-like peptide-1 (GLP-1) are produced from proglucagon through proteolytic cleavage. Blocking glucagon action increases the circulating levels of glucagon and GLP-1, reduces the blood glucose level, and induces the proliferation of islet α-cells. Glucagon blockade also suppresses hepatic amino acid catabolism and increases the serum amino acid level. In animal models defective in both glucagon and GLP-1, the blood glucose level is not reduced, indicating that GLP-1 is required for glucagon blockade to reduce the blood glucose level. In contrast, hyperplasia of α-cells and hyperaminoacidemia are observed in such animal models, indicating that GLP-1 is not required for the regulation of α-cell proliferation or amino acid metabolism. These findings suggest that the regulation of amino acid metabolism is a more important specific physiological role of glucagon than the regulation of glucose metabolism. Although the effects of glucagon deficiency on glucose metabolism are compensated by the suppression of insulin secretion, the effects on amino acid metabolism are not. Recently, data showing a feedback regulatory mechanism between the liver and islet α-cells, which is mediated by glucagon and amino acids, are accumulating. However, a number of questions on the mechanism of this regulation remain to be addressed. The profile of glucagon as a regulator of amino acid metabolism must be carefully considered for glucagon blockade to be applied therapeutically in the treatment of patients with diabetes.
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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.