ArticleThe Journal of physiology1999
Effects of calcium buffering on glucose-induced insulin release in mouse pancreatic islets: an approximation to the calcium sensor.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 32 citations in OpenAlex.
- Septin5 deletion enhances β-cell exocytosis by releasing microtubule-tethered insulin granules onto plasma membrane.Nature communications · 2025Article
- Disturbances in system dynamics ofJournal of bioenergetics and biomembranes · 2023Article
- CaAmerican journal of physiology. Endocrinology and metabolism · 2023Review
- Article
- 'Resistance is futile?' - paradoxical inhibitory effects of KThe Journal of physiology · 2020Review
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Ca2+ channel clustering with insulin-containing granules is disturbed in type 2 diabetes.The Journal of clinical investigation · 2017Article
- Model for glucagon secretion by pancreatic α-cells.PloS one · 2012Article
- Pancreatic islet cells: a model for calcium-dependent peptide release.HFSP journal · 2010Article
- Chronic palmitate exposure inhibits insulin secretion by dissociation of Ca(2+) channels from secretory granules.Cell metabolism · 2009Article
- Hyperinsulinism and diabetes: genetic dissection of beta cell metabolism-excitation coupling in mice.Cell metabolism · 2009Review
- Ca2+ dependency of 'Ca2+-independent' exocytosis in SPOC1 airway goblet cells.The Journal of physiology · 2004Article
- Nutrient toxicity in pancreatic beta-cell dysfunction.Journal of physiology and biochemistry · 2000Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The properties of the calcium sensor for glucose-induced insulin secretion have been studied using cell-permeant Ca2+ buffers with distinct kinetics and affinities. In addition, submembrane cytosolic Ca2+ distribution has been modelled after trains of glucose-induced action potential-like depolarizations. 2. Slow Ca2+ buffers (around 1 mmol l-1 intracellular concentration) with different affinities (EGTA and Calcium Orange-5N) did not significantly affect glucose-induced insulin release. Modelling showed no effect on cytosolic Ca2+ concentrations at the outermost shell (0.05 microm), their effects being observed in the innermost shells dependent on Ca2+ affinity. 3. In contrast, fast Ca2+ buffers (around 1 mmol l-1 intracellular concentration) with different affinities (BAPTA and Calcium Green-5N) caused a 50 % inhibition of early insulin response and completely blocked the late phase of glucose-induced insulin response, their simulations showing a decrease of [Ca2+]i at both the inner and outermost shells. 4. These data are consistent with the existence in pancreatic beta-cells of a higher affinity Ca2+ sensor than that proposed for neurons. Moreover, these data are consistent with the proposed existence of two distinct pools of granules: (i) 'primed' vesicles, colocalized with Ca2+ channels and responsible of the first phase of insulin release; and (ii) 'reserved pool' vesicles, not colocalized and responsible for the second phase.
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