ArticleThe Journal of physiology2006
Rapid glucose sensing by protein kinase A for insulin exocytosis in mouse pancreatic islets.
Article in The Journal of physiology, 2006. 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, 73 citations in OpenAlex.
- Single-molecule analysis of intracellular insulin granule behavior and its application to analyzing cytoskeletal dependence and pathophysiological implications.Frontiers in physiology · 2023Article
- Repair of traumatic lesions to the plasmalemma of neurons and other cells: Commonalities, conflicts, and controversies.Frontiers in physiology · 2023Review
- Intra-islet glucagon confers β-cell glucose competence for first-phase insulin secretion and favors GLP-1R stimulation by exogenous glucagon.The Journal of biological chemistry · 2022Article
- Overexpression of native IF1 downregulates glucose-stimulated insulin secretion by pancreatic INS-1E cells.Scientific reports · 2020Article
- Article
- Rp-cAMPS Prodrugs Reveal the cAMP Dependence of First-Phase Glucose-Stimulated Insulin Secretion.Molecular endocrinology (Baltimore, Md.) · 2015Article
- New insights concerning the molecular basis for defective glucoregulation in soluble adenylyl cyclase knockout mice.Biochimica et biophysica acta · 2014Review
- Activators of PKA and Epac distinctly influence insulin secretion and cytosolic Ca2+ in female mouse islets stimulated by glucose and tolbutamide.Endocrinology · 2014Article
- Phospholipase C-related catalytically inactive protein (PRIP) controls KIF5B-mediated insulin secretion.Biology open · 2014Article
- Molecular mechanisms underlying physiological and receptor pleiotropic effects mediated by GLP-1R activation.British journal of pharmacology · 2014Review
- In scarcity and abundance: metabolic signals regulating cell growth.Physiology (Bethesda, Md.) · 2013Review
- β-Cell-specific protein kinase A activation enhances the efficiency of glucose control by increasing acute-phase insulin secretion.Diabetes · 2013Article
- cAMP-mediated stabilization of fusion pores in cultured rat pituitary lactotrophs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Mathematical modeling of insulin secretion and the role of glucose-dependent mobilization, docking, priming and fusion of insulin granules.Journal of theoretical biology · 2013Article
- Cyclic AMP dynamics in the pancreatic β-cell.Upsala journal of medical sciences · 2012Review
- Anchored phosphatases modulate glucose homeostasis.The EMBO journal · 2012Article
- Modulation of dynamin-related protein 1 (DRP1) function by increased O-linked-β-N-acetylglucosamine modification (O-GlcNAc) in cardiac myocytes.The Journal of biological chemistry · 2012Article
- Coupling of metabolic, second messenger pathways and insulin granule dynamics in pancreatic beta-cells: a computational analysis.Progress in biophysics and molecular biology · 2011Review
- Molecular physiology of glucagon-like peptide-1 insulin secretagogue action in pancreatic β cells.Progress in biophysics and molecular biology · 2011Review
- Snapin mediates incretin action and augments glucose-dependent insulin secretion.Cell metabolism · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of protein kinase A (PKA) in insulin exocytosis was investigated with the use of two-photon excitation imaging of mouse islets of Langerhans. Inhibitors of PKA selectively reduced the number of exocytic events during the initial period (< 250 s) of the first phase of glucose-induced exocytosis (GIE), without affecting the second phase, in intact islets or small clusters of islet cells. The PKA inhibitors did not reduce the extent of the glucose-induced increase in [Ca(2+)](i). The actions of glucose and PKA in Ca(2+)-induced insulin exocytosis (CIE) triggered by photolysis of a caged-Ca(2+) compound, which resulted in large increases in [Ca(2+)](i) and thereby bypassed the ATP-sensitive K(+) channel-dependent mechanism of glucose sensing, were therefore studied. A high concentration (20 mM) of glucose potentiated CIE within 1 min, and this effect was blocked by inhibitors of PKA. This PKA-dependent action of glucose required glucose metabolism, given that increasing the intracellular concentration of cAMP by treatment with forskolin potentiated CIE only at the high glucose concentration. Finally, PKA appeared to reduce the frequency of 'kiss-and-run' exocytic events and to promote full-fusion events during GIE. These data indicate that a PKA-dependent mechanism of glucose sensing, which is operative even at the basal level of PKA activity, plays an important role specifically in the first phase of GIE, and they suggest that the action of PKA is mediated at the level of the fusion reaction.
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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.