Evidence map›Paper›PMID 16581855›Full record

ArticleThe Journal of physiology2006

Glucagon activates Ca2+ and Cl- channels in rat hepatocytes.

Edoardo C Aromataris, Michael L Roberts, Greg J Barritt, Grigori Y Rychkov

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-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

26 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Glucagon and Its Receptors in the Mammalian Heart.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin-1 via NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. TRPM2 channels mediate acetaminophen-induced liver damage.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  12. Article
  13. Bile formation and secretion.Comprehensive Physiology · 2013
    Review
  14. Cellular magnesium homeostasis.Archives of biochemistry and biophysics · 2011
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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 2 institutions in 1 country.

Edoardo C AromatarisSchool of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia.
Michael L Roberts
Greg J Barritt
Grigori Y Rychkov
University of Adelaide · AUFlinders University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucagon is one of the major hormonal regulators of glucose metabolism, counteracting the hepatic effects of insulin when the concentration of glucose in the bloodstream falls below a certain level. Glucagon also regulates bile flow, hepatocellular volume and membrane potential of hepatocytes. It is clear that changes in cell volume and membrane potential cannot occur without significant ion fluxes across the plasma membrane. The effects of glucagon on membrane currents in hepatocytes, however, are not well understood. Here we show, by patch-clamping of rat hepatocytes, that glucagon activates two types of currents: a small inwardly rectifying Ca2+ current with characteristics similar to those of the store-operated Ca2+ current and a larger outwardly rectifying Cl- current similar to that activated by cell swelling. We show that the mechanism of glucagon action on membrane conductance involves phospholipase C and adenylyl cyclase. Contribution of the adenylyl cyclase-dependent pathway to activation of the currents depended on Epac (exchange protein directly activated by cAMP), but not on protein kinase A. The activation of Ca2+ and Cl- channels is likely to play a key role in the mechanisms by which glucagon regulates hepatocyte metabolism and volume.

Indexed as

Chloride Channel AgonistsAdenineAdenylyl Cyclase InhibitorsAdenylyl CyclasesAnimalsCalciumCalcium Channel AgonistsCalcium ChannelsCell MembraneCells, CulturedChloride ChannelsChloridesCyclic AMPEstrenesGlucagonHepatocytes1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione9-(tetrahydro-2-furyl)-adenineAdenineAdenylyl Cyclase InhibitorsAdenylyl CyclasesCalciumCalcium Channel AgonistsCalcium ChannelsChloride Channel AgonistsChloride ChannelsChloridesCyclic AMPEstrenesGlucagonProtein Kinase InhibitorsPyrrolidinonesReceptors, GlucagonType C Phospholipases

Identifiers

PMID16581855
PMCPMC1779747
OpenAlexW1594572310

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.