Evidence map›Paper›PMID 24906950›Full record

ReviewDiabetologia2014

ATP-regulated potassium channels and voltage-gated calcium channels in pancreatic alpha and beta cells: similar functions but reciprocal effects on secretion.

Patrik Rorsman, Reshma Ramracheya, Nils J G Rorsman, Quan Zhang

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05616273 (Stimulated Glucagon as a Biomarker of Hypoglycemic Risk in Type 1 Diabetes), which is not on this map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
9.4field-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.

NCT05616273 completednot on this mapstarted 2023, after this paper: background citation

Stimulated Glucagon as a Biomarker of Hypoglycemic Risk in Type 1 Diabetes

TypeobservationalSponsorUniversity of ExeterRan2023 to 2025Enrolled62ConditionsType 1 Diabetes, HypoglycemiaArmsMixed Meal Tolerance Test (MMTT), Arginine Stimulation Test (AST), Home Finger Prick Sample
3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 94 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Investigation of Pancreatic-beta Cells Role in the Biological Process of Ageing.Endocrine, metabolic & immune disorders drug targets · 2024
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Role of ion channels in the mechanism of proteinuria (Review).Experimental and therapeutic medicine · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. The Glucagon-Like Adipokinetic Hormone inFrontiers in physiology · 2021
    Review
  20. 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

4 authors at 1 institution in 1 country.

Patrik RorsmanRadcliffe Department of Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, OX3 7LJ, UK, patrik.rorsman@drl.ox.ac.uk.
Reshma Ramracheya
Nils J G Rorsman
Quan Zhang
Oxford Centre for Diabetes, Endocrinology and Metabolism · GB

Funding

Medical Research CouncilWellcome Trust 084655Wellcome Trust 095531Wellcome Trust 095531/Z/11/Z
6 · The paper itself

Abstract

Closure of ATP-regulated K(+) channels (K(ATP) channels) plays a central role in glucose-stimulated insulin secretion in beta cells. K(ATP) channels are also highly expressed in glucagon-producing alpha cells, where their function remains unresolved. Under hypoglycaemic conditions, K(ATP) channels are open in alpha cells but their activity is low and only ~1% of that in beta cells. Like beta cells, alpha cells respond to hyperglycaemia with K(ATP) channel closure, membrane depolarisation and stimulation of action potential firing. Yet, hyperglycaemia reciprocally regulates glucagon (inhibition) and insulin secretion (stimulation). Here we discuss how this conundrum can be resolved and how reduced K(ATP) channel activity, via membrane depolarisation, paradoxically reduces alpha cell Ca(2+) entry and glucagon exocytosis. Finally, we consider whether the glucagon secretory defects associated with diabetes can be attributed to impaired K(ATP) channel regulation and discuss the potential for remedial pharmacological intervention using sulfonylureas.

Indexed as

AnimalsCalcium ChannelsDiabetes MellitusGlucagon-Secreting CellsHumansHypoglycemic AgentsInsulin-Secreting CellsKATP ChannelsSulfonylurea CompoundsCalcium ChannelsHypoglycemic AgentsKATP ChannelsSulfonylurea Compounds

Identifiers

PMID24906950
OpenAlexW2071824475

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.