Evidence map›Paper›PMID 25483880›Full record

ArticleIslets2014

Optogenetic control of insulin secretion in intact pancreatic islets with β-cell-specific expression of Channelrhodopsin-2.

Thomas M Reinbothe, Fatemeh Safi, Annika S Axelsson, Inês G Mollet, Anders H Rosengren

Open access · hybridAbstract read
In one paragraph

Article in Islets, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Light-stimulated insulin secretion from pancreatic islet-like organoids derived from human pluripotent stem cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  6. Dynamic changes in β-cell [CaMolecular metabolism · 2022
    Article
  7. Review
  8. Review
  9. Article
  10. Leader β-cells coordinate CaNature metabolism · 2019
    Article
  11. Sub-millisecond Control of Neuronal Firing by Organic Light-Emitting Diodes.Frontiers in bioengineering and biotechnology · 2019
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
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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

5 authors at 1 institution in 1 country.

Thomas M Reinbothea Department of Clinical Sciences; Lund University Diabetes Centre; Malmö, Sweden.
Fatemeh Safi
Annika S Axelsson
Inês G Mollet
Anders H Rosengren
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin is secreted from the pancreatic β-cells in response to elevated glucose. In intact islets the capacity for insulin release is determined by a complex interplay between different cell types. This has made it difficult to specifically assess the role of β-cell defects to the insulin secretory impairment in type 2 diabetes. Here we describe a new approach, based on optogenetics, that enables specific investigation of β-cells in intact islets. We used transgenic mice expressing the light-sensitive cation channel Channelrhodopsin-2 (ChR2) under control of the insulin promoter. Glucose tolerance in vivo was assessed using intraperitoneal glucose tolerance tests, and glucose-induced insulin release was measured from static batch incubations. ChR2 localization was determined by fluorescence confocal microscopy. The effect of ChR2 stimulation with blue LED light was assessed using Ca(2+) imaging and static islet incubations. Light stimulation of islets from transgenic ChR2 mice triggered prompt increases in intracellular Ca(2+). Moreover, light stimulation enhanced insulin secretion in batch-incubated islets at low and intermediate but not at high glucose concentrations. Glucagon release was not affected. Beta-cells from mice rendered diabetic on a high-fat diet exhibited a 3.5-fold increase in light-induced Ca(2+) influx compared with mice on a control diet. Furthermore, light enhanced insulin release also at high glucose in these mice, suggesting that high-fat feeding leads to a compensatory potentiation of the Ca(2+) response in β-cells. The results demonstrate the usefulness and versatility of optogenetics for studying mechanisms of perturbed hormone secretion in diabetes with high time-resolution and cell-specificity.

Indexed as

OptogeneticsAnimalsBacterial ProteinsCells, CulturedCell TrackingChannelrhodopsinsInsulinInsulin-Secreting CellsInsulin SecretionLuminescent ProteinsMiceMice, TransgenicOrgan SpecificityPromoter Regions, GeneticTransgenesBacterial ProteinsChannelrhodopsinsInsulinLuminescent Proteinsyellow fluorescent protein, Bacteriabeta-cellsChannelrhodopsin-2diabetesinsulin secretionisletsoptogenetics

Identifiers

PMID25483880
PMCPMC4593566
OpenAlexW2147245850

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.