ArticleThe Journal of physiology1995
Coincidence of early glucose-induced depolarization with lowering of cytoplasmic Ca2+ in mouse pancreatic beta-cells.
Article in The Journal of physiology, 1995. 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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21 citing papers in PubMed, 60 citations in OpenAlex.
- TMEM55A-mediated PI5P signalling regulates alpha cell actin depolymerisation and glucagon secretion.Diabetologia · 2025Article
- CaAmerican journal of physiology. Endocrinology and metabolism · 2023Review
- Fresh and cultured mouse islets differ in their response to nutrient stimulation.Endocrine connections · 2020Article
- Stromal Interaction Molecule 1 (STIM1) Regulates ATP-sensitive Potassium (The Journal of biological chemistry · 2017Article
- Fluorescent protein vectors for pancreatic islet cell identification in live-cell imaging.Pflugers Archiv : European journal of physiology · 2016Article
- Glucose control of glucagon secretion-'There's a brand-new gimmick every year'.Upsala journal of medical sciences · 2016Review
- Glucose Evokes Rapid Ca2+ and Cyclic AMP Signals by Activating the Cell-Surface Glucose-Sensing Receptor in Pancreatic β-Cells.PloS one · 2015Article
- Oscillations of sub-membrane ATP in glucose-stimulated beta cells depend on negative feedback from Ca(2+).Diabetologia · 2013Article
- cAMP induces stromal interaction molecule 1 (STIM1) puncta but neither Orai1 protein clustering nor store-operated Ca2+ entry (SOCE) in islet cells.The Journal of biological chemistry · 2012Article
- The mitochondrial Ca2+ uniporter MCU is essential for glucose-induced ATP increases in pancreatic β-cells.PloS one · 2012Article
- Ionic mechanisms and Ca2+ dynamics underlying the glucose response of pancreatic β cells: a simulation study.The Journal of general physiology · 2011Article
- Insulin secretion from beta-cells is affected by deletion of nicotinamide nucleotide transhydrogenase.Methods in enzymology · 2009Article
- Ca2+ controls slow NAD(P)H oscillations in glucose-stimulated mouse pancreatic islets.The Journal of physiology · 2006Article
- Loperamide mobilizes intracellular Ca2+ stores in insulin-secreting HIT-T15 cells.British journal of pharmacology · 2003Article
- Glucose-dependent regulation of rhythmic action potential firing in pancreatic beta-cells by K(ATP)-channel modulation.The Journal of physiology · 2002Article
- Association of upregulated activity of K(ATP) channels with impaired insulin secretion in UCP1-expressing insulinoma cells.The Journal of physiology · 2002Article
- The endoplasmic reticulum is a glucose-modulated high-affinity sink for Ca2+ in mouse pancreatic beta-cells.The Journal of physiology · 2001Article
- Localized calcium influx in pancreatic beta-cells: its significance for Ca2+-dependent insulin secretion from the islets of Langerhans.Endocrine · 2000Review
- cAMP-dependent mobilization of intracellular Ca2+ stores by activation of ryanodine receptors in pancreatic beta-cells. A Ca2+ signaling system stimulated by the insulinotropic hormone glucagon-like peptide-1-(7-37).The Journal of biological chemistry · 1999Article
- Glucose diffusion in pancreatic islets of Langerhans.Biophysical journal · 1998Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The temporal relationship between the early glucose-induced changes of membrane potential and cytoplasmic Ca2+ concentration ([Ca2+]i) was studied in insulin-releasing pancreatic beta-cells. 2. The mean resting membrane potential and [Ca2+]i were about -70 mV and 60 nM, respectively, in 3 mM glucose. 3. Elevating the glucose concentration to 8-23 mM typically elicited a slow depolarization, which was paralleled by a lowering of [Ca2+]i. When the slow depolarization had reached a threshold of -55 to -40 mV, there was rapid further depolarization to a plateau with superimposed action potentials, and [Ca2+]i increased dramatically. 4. Imposing hyperpolarizations and depolarizations of 10 mV from a holding potential of -70 mV had no detectable effect on [Ca2+]i. Furthermore, glucose elevation elicited a decrease in [Ca2+]i even at a holding potential of -70 mV. 5. Step depolarizations induced [Ca2+]i transients, which decayed with time courses well fitted by double exponentials. The slower component became faster by a factor of about 4 upon elevation of glucose, suggesting involvement of ATP-dependent Ca2+ sequestration or extrusion of [Ca2+]i. 6. Glucose stimulation increased the size and accelerated the recovery of carbachol-triggered [Ca2+]i transients, and thapsigargin, an intracellular Ca(2+)-ATPase inhibitor, counteracted the glucose-induced lowering of [Ca2+]i, indicating that calcium transport into intracellular stores is involved in glucose-induced lowering of [Ca2+]i. 7. The results support the notion that in beta-cells, nutrient-induced elevation of ATP leads initially to ATP-dependent removal of Ca2+ from the cytoplasm, paralleled by a slow depolarization due to inhibition of ATP-sensitive K+ channels. Only after depolarization has reached a threshold do action potentials occur, inducing a sharp elevation in [Ca2+]i.
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