Evidence map›Paper›PMID 20862277›Full record

ArticlePloS one2010

New function for an old enzyme: NEP deficient mice develop late-onset obesity.

Matthias Becker, Wolf-Eberhard Siems, Reinhart Kluge, Florian Gembardt, Heinz-Peter Schultheiss, Michael Schirner, Thomas Walther

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. 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
0.8field-weighted citation impact, top 32% 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, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Association of Ang-(1-7) and des-ArgHypertension research : official journal of the Japanese Society of Hypertension · 2021
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  7. Review
  8. Article
  9. Review
  10. Article
  11. Is Entresto good for the brain?World journal of cardiology · 2017
    Review
  12. Article
  13. eLife · 2016
    Article
  14. Green tea reduces body fat via upregulation of neprilysin.International journal of obesity (2005) · 2016
    Article
  15. Review
  16. Article
  17. Article
  18. 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

7 authors at 5 institutions in 2 countries.

Matthias BeckerDepartment for Biochemical Neurobiology, Leibniz-Institut für Molekulare Pharmakologie, Berlin, Germany.
Wolf-Eberhard Siems
Reinhart Kluge
Florian Gembardt
Heinz-Peter Schultheiss
Michael Schirner
Thomas Walther
Leibniz-Forschungsinstitut für Molekulare Pharmakologie · DECharité - Universitätsmedizin Berlin · DEGerman Institute of Human Nutrition · DEHull York Medical School · GBUniversity of Hull · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccording to the World Health Organization (WHO) there is a pandemic of obesity with approximately 300 million people being obese. Typically, human obesity has a polygenetic causation. Neutral endopeptidase (NEP), also known as neprilysin, is considered to be one of the key enzymes in the metabolism of many active peptide hormones. METHODOLOGY/PRINCIPAL

findingsAn incidental observation in NEP-deficient mice was a late-onset excessive gain in body weight exclusively from a ubiquitous accumulation of fat tissue. In accord with polygenetic human obesity, mice were characterized by deregulation of lipid metabolism, higher blood glucose levels, with impaired glucose tolerance. The key role of NEP in determining body mass was confirmed by the use of the NEP inhibitor candoxatril in wild-type mice that increased body weight due to increased food intake. This is a peripheral and not a central NEP action on the switch for appetite control, since candoxatril cannot cross the blood-brain barrier. Furthermore, we demonstrated that inhibition of NEP in mice with cachexia delayed rapid body weight loss. Thus, lack in NEP activity, genetically or pharmacologically, leads to a gain in body fat. CONCLUSIONS/SIGNIFICANCE: In the present study, we have identified NEP to be a crucial player in the development of obesity. NEP-deficient mice start to become obese under a normocaloric diet in an age of 6-7 months and thus are an ideal model for the typical human late-onset obesity. Therefore, the described obesity model is an ideal tool for research on development, molecular mechanisms, diagnosis, and therapy of the pandemic obesity.

Indexed as

Adipose TissueAge of OnsetAnimalsBlood GlucoseDisease Models, AnimalMiceMice, KnockoutNeprilysinObesityWeight GainBlood GlucoseNeprilysin

Identifiers

PMID20862277
PMCPMC2940827
OpenAlexW2092611703

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.