Evidence map›Paper›PMID 28591164›Full record

ArticlePloS one2017

Alamandine reduces leptin expression through the c-Src/p38 MAP kinase pathway in adipose tissue.

Tsuyoshi Uchiyama, Fumikazu Okajima, Chihiro Mogi, Ayaka Tobo, Shoichi Tomono, Koichi Sato

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 40 citations in OpenAlex.

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  13. The antiobese effect of AT1 receptor blockade is augmented in mice lacking Mas.Naunyn-Schmiedeberg's archives of pharmacology · 2019
    Article
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  15. The renin-angiotensin system: going beyond the classical paradigms.American journal of physiology. Heart and circulatory physiology · 2019
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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

6 authors at 2 institutions in 1 country.

Tsuyoshi UchiyamaLaboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.ORCID http://orcid.org/0000-0002-5967-8516
Fumikazu OkajimaAomori University, Faculty of Pharmaceutical Sciences, Aomori, Japan.
Chihiro MogiLaboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
Ayaka ToboLaboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
Shoichi TomonoGunma University School of Health Sciences, Maebashi, Gunma, Japan.
Koichi SatoLaboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
Gunma University · JPAomori University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveObesity is associated with an increased risk of diabetes mellitus, hypertension, and renal dysfunction. Angiotensin 1-7 and alamandine are heptameric renin angiotensin system peptide hormones. Further, alamandine levels increase with renal dysfunction. In the cardiovascular system, angiotensin 1-7 and alamandine produce similar improvements and counterbalance angiotensin II in regulating vascular function. We aimed to determine whether the effect of alamandine on leptin expression and secretion in adipocytes was similar to that of angiotensin 1-7. APPROACH AND

resultsWe studied isolated peri-renal visceral adipose tissue and peri-renal isolated visceral adipocytes from male Wistar rats. Angiotensin II from 0.01 to 10nM had no effect on leptin expression. Angiotensin 1-7 (1 nM) increased leptin secretion and expression, whereas alamandine (1 nM) decreased leptin secretion and expression in adipose tissue and isolated adipocytes and reduced blood leptin levels in vivo. These effects were mediated by Gq, c-Src, p38 mitogen-activated protein, and IκB activation. Additionally, alamandine induced nitric oxide expression via inducible nitric oxidase synthase and plasminogen activator inhibitor 1 expression in adipose tissue and isolated adipocytes.

conclusionsAngiotensin 1-7 and alamandine produced opposing effects on leptin expression and secretion in adipose tissue. This result suggests that the action of Mas (angiotensin 1-7 receptor) and Mas-related G-protein coupled receptor D in adipocytes exhibited opposing actions similar to angiotensin II type 1 and type 2 receptors.

Indexed as

3T3-L1 CellsAdipocytesAdipose TissueAngiotensin IAnimalsCell SeparationCSK Tyrosine-Protein KinaseGTP-Binding Protein alpha Subunits, Gq-G11LeptinMaleMAP Kinase Signaling SystemMiceModels, BiologicalNF-kappa BNitric OxideNitric Oxide Synthase Type IIalamandineAngiotensin Iangiotensin I (1-7)CSK Tyrosine-Protein KinaseGTP-Binding Protein alpha Subunits, Gq-G11LeptinMas-related receptor MrgD, ratNF-kappa BNitric OxideNitric Oxide Synthase Type IIOligopeptidesPeptide FragmentsPlasminogen Activator Inhibitor 1Receptors, G-Protein-Coupledsrc-Family Kinases

Identifiers

PMID28591164
PMCPMC5462406
OpenAlexW2623827740

What OpenQuestion holds

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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.