Evidence map›Paper›PMID 29062272›Full record

ArticleFrontiers in cellular neuroscience2017

Obesity Increases Mitogen-Activated Protein Kinase Phosphatase-3 Levels in the Hypothalamus of Mice.

Bárbara de A Rodrigues, Vitor R Muñoz, Gabriel K Kuga, Rafael C Gaspar, Susana C B R Nakandakari, Barbara M Crisol, José D Botezelli, Luciana S S Pauli, Adelino S R da Silva, Leandro P de Moura and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. MAP kinase phosphatases in metabolic diseases.Trends in endocrinology and metabolism: TEM · 2026
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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

13 authors at 2 institutions in 1 country.

Bárbara de A RodriguesLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Vitor R MuñozLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Gabriel K KugaLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Rafael C GasparLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Susana C B R NakandakariOCRC-Obesity and Comorbidities Research Center, University of Campinas (UNICAMP), São Paulo, Brazil.
Barbara M CrisolLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
José D BotezelliLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Luciana S S PauliLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Adelino S R da SilvaSchool of Physical Education and Sport of Ribeirão Preto, University of São Paulo (USP), São Paulo, Brazil.
Leandro P de MouraLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Dennys E CintraOCRC-Obesity and Comorbidities Research Center, University of Campinas (UNICAMP), São Paulo, Brazil.
Eduardo R RopelleLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
José R PauliLaboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Universidade Estadual de Campinas (UNICAMP) · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitogen-activated Protein Kinase Phosphatase 3 (MKP-3) has been involved in the negative regulation of insulin signaling. The absence of MKP-3 is also associated with reduced adiposity, increased energy expenditure and improved insulin sensitivity. The MKP-3 is known as the main Erk1/2 phosphatase and FoxO1 activator, which has repercussions on the gluconeogenesis pathway and hyperglycemia in obese mice. Recently, we showed that MKP-3 overexpression decreases FoxO1 phosphorylation in the hypothalamus of lean mice. However, the hypothalamic interaction between MKP-3 and FoxO1 during obesity was not investigated yet. Here, the MKP-3 expression and the effects on food intake and energy expenditure, were investigated in high-fat diet-induced obese mice. The results indicate that obesity in mice increased the MKP-3 protein content in the hypothalamus. This hypothalamic upregulation led to an increase of food intake, adiposity, and body weight. Furthermore, the obese mice with increased MKP-3 showed an insulin signaling impairment with reduction of insulin-induced FoxO1 and Erk1/2 phosphorylation in the hypothalamus. Moreover, a bioinformatics analysis of data demonstrated that hypothalamic MKP-3 mRNA levels were positively correlated with body weight and negatively correlated to oxygen consumption (VO

Indexed as

food intakehypothalamusinsulinMKP-3obesity

Identifiers

PMID29062272
PMCPMC5640777
OpenAlexW2761719371

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.