Evidence map›Paper›PMID 19401420›Full record

ArticleDiabetes2009

Inhibitory effects of leptin on pancreatic alpha-cell function.

Eva Tudurí, Laura Marroquí, Sergi Soriano, Ana B Ropero, Thiago M Batista, Sandra Piquer, Miguel A López-Boado, Everardo M Carneiro, Ramón Gomis, Angel Nadal and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 77 citations in OpenAlex.

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  13. The glucoregulatory actions of leptin.Molecular metabolism · 2017
    Review
  14. Glucagon increase after chronic ATNaunyn-Schmiedeberg's archives of pharmacology · 2017
    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

11 authors at 3 institutions in 1 country.

Eva TuduríInstituto de Bioingeniería, Universidad Miguel Hernandez, Elche, Spain.
Laura Marroquí
Sergi Soriano
Ana B Ropero
Thiago M Batista
Sandra Piquer
Miguel A López-Boado
Everardo M Carneiro
Ramón Gomis
Angel Nadal
Ivan Quesada
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESUniversitat de Miguel Hernández d'Elx · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveLeptin released from adipocytes plays a key role in the control of food intake, energy balance, and glucose homeostasis. In addition to its central action, leptin directly affects pancreatic beta-cells, inhibiting insulin secretion, and, thus, modulating glucose homeostasis. However, despite the importance of glucagon secretion in glucose homeostasis, the role of leptin in alpha-cell function has not been studied in detail. In the present study, we have investigated this functional interaction. RESEARCH DESIGN AND

methodsThe presence of leptin receptors (ObR) was demonstrated by RT-PCR analysis, Western blot, and immunocytochemistry. Electrical activity was analyzed by patch-clamp and Ca(2+) signals by confocal microscopy. Exocytosis and glucagon secretion were assessed using fluorescence methods and radioimmunoassay, respectively.

resultsThe expression of several ObR isoforms (a-e) was detected in glucagon-secreting alphaTC1-9 cells. ObRb, the main isoform involved in leptin signaling, was identified at the protein level in alphaTC1-9 cells as well as in mouse and human alpha-cells. The application of leptin (6.25 nmol/l) hyperpolarized the alpha-cell membrane potential, suppressing the electrical activity induced by 0.5 mmol/l glucose. Additionally, leptin inhibited Ca(2+) signaling in alphaTC1-9 cells and in mouse and human alpha-cells within intact islets. A similar result occurred with 0.625 nmol/l leptin. These effects were accompanied by a decrease in glucagon secretion from mouse islets and were counteracted by the phosphatidylinositol 3-kinase inhibitor, wortmannin, suggesting the involvement of this pathway in leptin action.

conclusionsThese results demonstrate that leptin inhibits alpha-cell function, and, thus, these cells are involved in the adipoinsular communication.

Indexed as

AnimalsCalciumCells, CulturedExocytosisGlucagonGlucagon-Secreting CellsImmunohistochemistryLeptinMiceMice, Inbred StrainsMicroscopy, ConfocalReceptors, LeptinReverse Transcriptase Polymerase Chain ReactionRNASignal TransductionCalciumGlucagonLeptinReceptors, LeptinRNA

Identifiers

PMID19401420
PMCPMC2699864
OpenAlexW2154039375

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.