Evidence map›Paper›PMID 19855088›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2009

Rapid regulation of K(ATP) channel activity by 17{beta}-estradiol in pancreatic {beta}-cells involves the estrogen receptor {beta} and the atrial natriuretic peptide receptor.

Sergi Soriano, Ana B Ropero, Paloma Alonso-Magdalena, Cristina Ripoll, Ivan Quesada, Birgit Gassner, Michaela Kuhn, Jan-Ake Gustafsson, Angel Nadal

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 94 citations in OpenAlex.

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  9. Metabolic responses to intermittent hypoxia are regulated by sex and estradiol in mice.American journal of physiology. Endocrinology and metabolism · 2021
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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

9 authors at 4 institutions in 4 countries.

Sergi SorianoInstitute of Bioengineering and CIBERDEM, Universidad Miguel Hernández de Elche, Alicante, Spain.
Ana B Ropero
Paloma Alonso-Magdalena
Cristina Ripoll
Ivan Quesada
Birgit Gassner
Michaela Kuhn
Jan-Ake Gustafsson
Angel Nadal
Universitat de Miguel Hernández d'Elx · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESUniversity of Würzburg · DEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ATP-sensitive potassium (K(ATP)) channel is a key molecule involved in glucose-stimulated insulin secretion. The activity of this channel regulates beta-cell membrane potential, glucose- induced [Ca(2+)](i) signals, and insulin release. In this study, the rapid effect of physiological concentrations of 17beta-estradiol (E2) on K(ATP) channel activity was studied in intact beta-cells by use of the patch-clamp technique. When cells from wild-type (WT) mice were used, 1 nm E2 rapidly reduced K(ATP) channel activity by 60%. The action of E2 on K(ATP) channel was not modified in beta-cells from ERalpha-/- mice, yet it was significantly reduced in cells from ERbeta-/- mice. The effect of E2 was mimicked by the ERbeta agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN). Activation of ERbeta by DPN enhanced glucose-induced Ca(2+) signals and insulin release. Previous evidence indicated that the acute inhibitory effects of E2 on K(ATP) channel activity involve cyclic GMP and cyclic GMP-dependent protein kinase. In this study, we used beta-cells from mice with genetic ablation of the membrane guanylate cyclase A receptor for atrial natriuretic peptide (also called the atrial natriuretic peptide receptor) (GC-A KO mice) to demonstrate the involvement of this membrane receptor in the rapid E2 actions triggered in beta-cells. E2 rapidly inhibited K(ATP) channel activity and enhanced insulin release in islets from WT mice but not in islets from GC-A KO mice. In addition, DPN reduced K(ATP) channel activity in beta-cells from WT mice, but not in beta-cells from GC-A KO mice. This work unveils a new role for ERbeta as an insulinotropic molecule that may have important physiological and pharmacological implications.

Indexed as

AnimalsCalciumCells, CulturedEstradiolEstrogen Receptor alphaEstrogen Receptor betaFemaleImmunohistochemistryInsulin-Secreting CellsKATP ChannelsMiceMice, KnockoutNitrilesPatch-Clamp TechniquesPhenolsPropionates2,3-bis(4-hydroxyphenyl)-propionitrile4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenolCalciumEstradiolEstrogen Receptor alphaEstrogen Receptor betaKATP ChannelsNitrilesPhenolsPropionatesPyrazolesReceptors, Atrial Natriuretic Factor

Identifiers

PMID19855088
PMCPMC5419133
OpenAlexW2077411765

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.