Evidence map›Paper›PMID 14966302›Full record

ArticleThe Journal of physiology2004

Capacitance measurements of exocytosis in mouse pancreatic alpha-, beta- and delta-cells within intact islets of Langerhans.

Sven Göpel, Quan Zhang, Lena Eliasson, Xiao-Song Ma, Juris Galvanovskis, Takahiro Kanno, Albert Salehi, Patrik Rorsman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
9.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

83 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Loss of tetraspanin-7 expression reduces pancreatic β-cell exocytosis CaDiabetic medicine : a journal of the British Diabetic Association · 2022
    Article
  7. Review
  8. Review
  9. Dynamin deficiency causes insulin secretion failure and hyperglycemia.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Review
  11. Review
  12. CaChannels (Austin, Tex.) · 2020
    Review
  13. Article
  14. Review
  15. Cellular and systemic mechanisms for glucose sensing and homeostasis.Pflugers Archiv : European journal of physiology · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

23 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Sven GöpelDepartment of Physiological Sciences, BMC F11, SE-221 84 Lund, Sweden.
Quan Zhang
Lena Eliasson
Xiao-Song Ma
Juris Galvanovskis
Takahiro Kanno
Albert Salehi
Patrik Rorsman
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Capacitance measurements of exocytosis were applied to functionally identified alpha-, beta- and delta-cells in intact mouse pancreatic islets. The maximum rate of capacitance increase in beta-cells during a depolarization to 0 mV was equivalent to 14 granules s(-1), <5% of that observed in isolated beta-cells. Beta-cell secretion exhibited bell-shaped voltage dependence and peaked at +20 mV. At physiological membrane potentials (up to approximately -20 mV) the maximum rate of release was approximately 4 granules s(-1). Both exocytosis (measured by capacitance measurements) and insulin release (detected by radioimmunoassay) were strongly inhibited by the L-type Ca(2+) channel blocker nifedipine (25 microm) but only marginally (<20%) affected by the R-type Ca(2+) channel blocker SNX482 (100 nm). Exocytosis in the glucagon-producing alpha-cells peaked at +20 mV. The capacitance increases elicited by pulses to 0 mV exhibited biphasic kinetics and consisted of an initial transient (150 granules s(-1)) and a sustained late component (30 granules s(-1)). Whereas addition of the N-type Ca(2+) channel blocker omega-conotoxin GVIA (0.1 microm) inhibited glucagon secretion measured in the presence of 1 mm glucose to the same extent as an elevation of glucose to 20 mm, the L-type Ca(2+) channel blocker nifedipine (25 microm) had no effect. Thus, glucagon release during hyperglycaemic conditions depends principally on Ca(2+)-influx through N-type rather than L-type Ca(2+) channels. Exocytosis in the somatostatin-secreting delta-cells likewise exhibited two kinetically separable phases of capacitance increase and consisted of an early rapid (600 granules s(-1)) component followed by a sustained slower (60 granules s(-1)) component. We conclude that (1) capacitance measurements in intact pancreatic islets are feasible; (2) exocytosis measured in beta-cells in situ is significantly slower than that of isolated cells; and (3) the different types of islet cells exhibit distinct exocytotic features.

Indexed as

Electric CapacitanceAction PotentialsAnimalsCalcium Channels, L-TypeCalcium Channels, N-TypeCalcium Channels, R-TypeCells, CulturedElectrophysiologyExocytosisGlucagonGlucoseInsulinInsulin SecretionIslets of LangerhansKineticsMembrane PotentialsCalcium Channels, L-TypeCalcium Channels, N-TypeCalcium Channels, R-TypeGlucagonGlucoseInsulinNifedipineomega-Conotoxin GVIAPertussis ToxinSNX 482Spider Venoms

Identifiers

PMID14966302
PMCPMC1664984
OpenAlexW1562853684

What OpenQuestion holds

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Registered trials

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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.