ArticleAmerican journal of physiology. Cell physiology2007
Regulation of cAMP dynamics by Ca2+ and G protein-coupled receptors in the pancreatic beta-cell: a computational approach.
Article in American journal of physiology. Cell physiology, 2007. 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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31 citing papers in PubMed, 67 citations in OpenAlex.
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- Regulator of G-protein signaling Gβ5-R7 is a crucial activator of muscarinic M3 receptor-stimulated insulin secretion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Regulation of Glucokinase by Intracellular Calcium Levels in Pancreatic β Cells.The Journal of biological chemistry · 2016Article
- Pancreatic Beta Cell G-Protein Coupled Receptors and Second Messenger Interactions: A Systems Biology Computational Analysis.PloS one · 2016Article
- Transient Receptor Potential Vanilloid 4-Induced Modulation of Voltage-Gated Sodium Channels in Hippocampal Neurons.Molecular neurobiology · 2016Article
- Modeling of glucose-induced cAMP oscillations in pancreatic β cells: cAMP rocks when metabolism rolls.Biophysical journal · 2015Article
- Rp-cAMPS Prodrugs Reveal the cAMP Dependence of First-Phase Glucose-Stimulated Insulin Secretion.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Glucose Evokes Rapid Ca2+ and Cyclic AMP Signals by Activating the Cell-Surface Glucose-Sensing Receptor in Pancreatic β-Cells.PloS one · 2015Article
- New insights concerning the molecular basis for defective glucoregulation in soluble adenylyl cyclase knockout mice.Biochimica et biophysica acta · 2014Review
- Cellular communication and heterogeneity in pancreatic islet insulin secretion dynamics.Trends in endocrinology and metabolism: TEM · 2014Review
- Virtual Systems Pharmacology (ViSP) software for simulation from mechanistic systems-level models.Frontiers in pharmacology · 2014Article
- Cyclic AMP dynamics in the pancreatic β-cell.Upsala journal of medical sciences · 2012Review
- Glucose-dependent insulinotropic polypeptide signaling in pancreatic β-cells and adipocytes.Journal of diabetes investigation · 2012Review
- SUMO downregulates GLP-1-stimulated cAMP generation and insulin secretion.American journal of physiology. Endocrinology and metabolism · 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
- Glucose- and hormone-induced cAMP oscillations in α- and β-cells within intact pancreatic islets.Diabetes · 2011Article
- Adenylyl cyclase 8 is central to glucagon-like peptide 1 signalling and effects of chronically elevated glucose in rat and human pancreatic beta cells.Diabetologia · 2011Article
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4 authors at 1 institution in 1 country.
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Abstract
In this report we describe a mathematical model for the regulation of cAMP dynamics in pancreatic beta-cells. Incretin hormones such as glucagon-like peptide 1 (GLP-1) increase cAMP and augment insulin secretion in pancreatic beta-cells. Imaging experiments performed in MIN6 insulinoma cells expressing a genetically encoded cAMP biosensor and loaded with fura-2, a calcium indicator, showed that cAMP oscillations are differentially regulated by periodic changes in membrane potential and GLP-1. We modeled the interplay of intracellular calcium (Ca(2+)) and its interaction with calmodulin, G protein-coupled receptor activation, adenylyl cyclases (AC), and phosphodiesterases (PDE). Simulations with the model demonstrate that cAMP oscillations are coupled to cytoplasmic Ca(2+) oscillations in the beta-cell. Slow Ca(2+) oscillations (<1 min(-1)) produce low-frequency cAMP oscillations, and faster Ca(2+) oscillations (>3-4 min(-1)) entrain high-frequency, low-amplitude cAMP oscillations. The model predicts that GLP-1 receptor agonists induce cAMP oscillations in phase with cytoplasmic Ca(2+) oscillations. In contrast, observed antiphasic Ca(2+) and cAMP oscillations can be simulated following combined glucose and tetraethylammonium-induced changes in membrane potential. The model provides additional evidence for a pivotal role for Ca(2+)-dependent AC and PDE activation in coupling of Ca(2+) and cAMP signals. Our results reveal important differences in the effects of glucose/TEA and GLP-1 on cAMP dynamics in MIN6 beta-cells.
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