Evidence map›Paper›PMID 11080250›Full record

ReviewThe Journal of physiology2000

Mitochondrial signals in glucose-stimulated insulin secretion in the beta cell.

P Maechler, C B Wollheim

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
10.1field-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

46 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Dysfunctions, molecular mechanisms, and therapeutic strategies of pancreatic β-cells in diabetes.Apoptosis : an international journal on programmed cell death · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Bisphenol A and Type 2 Diabetes Mellitus: A Review of Epidemiologic, Functional, and Early Life Factors.International journal of environmental research and public health · 2021
    Review
  13. Management of mitochondrial diabetes in the era of novel therapies.Journal of diabetes and its complications · 2021
    Article
  14. Review
  15. Control by CaCell calcium · 2020
    Review
  16. NADSignal transduction and targeted therapy · 2020
    Review
  17. Article
  18. Analysis of Non-Human Primate Pancreatic Islet Oxygen Consumption.Journal of visualized experiments : JoVE · 2019
    Article
  19. ATP-sensitive KPflugers Archiv : European journal of physiology · 2019
    Article
  20. Glycogen Synthase Kinase 3 Beta Controls Presenilin-1-Mediated Endoplasmic Reticulum Ca²⁺ Leak Directed to Mitochondria in Pancreatic Islets and β-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019
    Article
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

2 authors.

P MaechlerDivision of Clinical Biochemistry, Department of Internal Medicine, University Medical Center, 1211 Geneva 4, Switzerland.
C B Wollheim

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose-induced insulin secretion is determined by signals generated in the mitochondria. The elevation of ATP is necessary for the membrane-dependent increase in cytosolic Ca2+, the main trigger of insulin exocytosis. Beta cells depleted of mitochondrial DNA fail to respond to glucose while still secreting insulin in response to membrane depolarisation. This cell model resembles the situation of defective insulin secretion in patients with mitochondrial diabetes. On the other hand, infants with activating mutations in the mitochondrial enzyme glutamate dehydrogenase are characterised by hyperinsulinism and hypoglycaemia. We have recently proposed that glutamate, generated by this enzyme, participates in insulin secretion as a glucose-derived metabolic messenger. In this model, glutamate acts downstream of the mitochondria by sensitising the exocytotic process to Ca2+. The evidence in favour of such a role for glutamate is discussed in the present review.

Indexed as

AnimalsExocytosisGlucoseHumansInsulinIslets of LangerhansMitochondriaSignal TransductionStimulation, ChemicalGlucoseInsulin

Identifiers

PMID11080250
PMCPMC2270172
OpenAlexW2053697597

What OpenQuestion holds

Textmetadata
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.