ArticleThe Journal of clinical investigation1993
Small elevations of glucose concentration redirect and amplify the synthesis of guanosine 5'-triphosphate in rat islets.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
21 citing papers in PubMed, 44 citations in OpenAlex.
- The RhoGDIβ-Rac1-CARD9 Signaling Module Mediates Islet β-Cell Dysfunction Under Chronic Hyperglycemia.Cells · 2025Review
- Underappreciated roles for Rho GDP dissociation inhibitors (RhoGDIs) in cell function: Lessons learned from the pancreatic islet β-cell.Biochemical pharmacology · 2022Review
- Review
- Paradoxical regulation of glucose-induced Rac1 activation and insulin secretion by RhoGDIβ in pancreatic β-cells.Small GTPases · 2021Article
- P-Rex1 Mediates Glucose-Stimulated Rac1 Activation and Insulin Secretion in Pancreatic β-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2020Article
- GPCRs, G Proteins, and Their Impact on β-cell Function.Comprehensive Physiology · 2020Review
- Nm23-H1 regulates glucose-stimulated insulin secretion in pancreatic β-cells via Arf6-Rac1 signaling axis.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2013Article
- Protein histidine [de]phosphorylation in insulin secretion: abnormalities in models of impaired insulin secretion.Naunyn-Schmiedeberg's archives of pharmacology · 2011Review
- A farnesylated G-protein suppresses Akt phosphorylation in INS 832/13 cells and normal rat islets: regulation by pertussis toxin and PGE₂.Biochemical pharmacology · 2011Article
- Phagocyte-like NADPH oxidase generates ROS in INS 832/13 cells and rat islets: role of protein prenylation.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Small G proteins in islet beta-cell function.Endocrine reviews · 2010Review
- Down-regulation of expression and function of nucleoside diphosphate kinase in insulin-secreting beta-cells under in vitro conditions of glucolipotoxicity.Molecular and cellular biochemistry · 2009Article
- Mechanisms of biphasic insulin-granule exocytosis - roles of the cytoskeleton, small GTPases and SNARE proteins.Journal of cell science · 2009Review
- Emerging roles for protein histidine phosphorylation in cellular signal transduction: lessons from the islet beta-cell.Journal of cellular and molecular medicine · 2008Review
- Bridging the gap between protein carboxyl methylation and phospholipid methylation to understand glucose-stimulated insulin secretion from the pancreatic beta cell.Biochemical pharmacology · 2008Review
- Aspects of novel sites of regulation of the insulin stimulus-secretion coupling in normal and diabetic pancreatic islets.Endocrine · 1998Review
- Glucose- and GTP-dependent stimulation of the carboxyl methylation of CDC42 in rodent and human pancreatic islets and pure beta cells. Evidence for an essential role of GTP-binding proteins in nutrient-induced insulin secretion.The Journal of clinical investigation · 1996Article
- A novel regulatory mechanism for trimeric GTP-binding proteins in the membrane and secretory granule fractions of human and rodent beta cells.The Biochemical journal · 1996Article
- Evidence of a role for GTP in the potentiation of Ca(2+)-induced insulin secretion by glucose in intact rat islets.The Journal of clinical investigation · 1995Article
- Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies suggest a permissive requirement for guanosine 5'-triphosphate (GTP) in insulin release, based on the use of GTP synthesis inhibitors (such as myocophenolic acid) acting at inosine monophosphate (IMP) dehydrogenase; herein, we examine the glucose dependency of GTP synthesis. Mycophenolic acid inhibited insulin secretion equally well after islet culture at 7.8 or 11.1 mM glucose (51% inhibition) but its effect was dramatically attenuated when provided at < or = 6.4 mM glucose (13% inhibition; P < 0.001). These observations were explicable by a stimulation of islet GTP synthesis derived from IMP since, at high glucose: (a) total GTP content was augmented; (b) a greater decrement in GTP (1.75 vs. 1.05 pmol/islet) was induced by mycophenolic acid; and (c) a smaller "pool" of residual GTP persisted after drug treatment. Glucose also accelerated GTP synthesis from exogenous guanine ("salvage" pathway) and increased content of a pyrimidine, uridine 5'-triphosphate (UTP), suggesting that glucose augments production of a common regulatory intermediate (probably 5-phosphoribosyl-1-pyrophosphate). Pathway-specific radiolabeling studies confirmed that glucose tripled both salvage and de novo synthesis of nucleotides. We conclude that steep changes in the biosynthesis of cytosolic pools of GTP occur at modest changes in glucose concentrations, a finding which may have relevance to the adaptive (patho) physiologic responses of islets to changes in ambient glucose levels.
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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.