Evidence map›Paper›PMID 28262782›Full record

ArticleScientific reports2017

Amyloid precursor protein modulates macrophage phenotype and diet-dependent weight gain.

Kendra L Puig, Stephen A Brose, Xudong Zhou, Mary A Sens, Gerald F Combs, Michael D Jensen, Mikhail Y Golovko, Colin K Combs

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Review
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  18. Dysregulated bile acid synthesis and dysbiosis are implicated in Western diet-induced systemic inflammation, microglial activation, and reduced neuroplasticity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  19. Review
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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

8 authors.

Kendra L PuigDepartment of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58202, USA.
Stephen A BroseDepartment of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58202, USA.
Xudong ZhouDepartment of Pathology, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58202, USA.
Mary A SensDepartment of Pathology, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58202, USA.
Gerald F CombsGrand Forks Human Nutrition Res. Center (GFHNRC), ARS-USDA, Grand Forks, ND 58201, USA.
Michael D JensenEndocrine Research Unit, Mayo Clinic, Rochester, MN 55905, USA.
Mikhail Y GolovkoDepartment of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58202, USA.
Colin K CombsDepartment of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58202, USA.

Funding

Yersina perstis interactions with macrophagesP20GM113123 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI BRADLEY, DAVID S. · 2016 to 2025
$19.9M
FFA METABOLISM IN DIFFERENT TYPES OF HUMAN OBESITYR01DK040484 · NIDDK · MAYO CLINIC ROCHESTER · PI MICHAEL D. JENSEN · 1993 to 2026
$8.2M
Pilot Projects CoreP30GM103329 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI GEIGER, JONATHAN DAVID · 2012 to 2016
$5.1M
Mechanisms of exposure-induced tissue functional and pathological changes in a mouse model of Alzheimer's DiseaseR01AG057046 · NIA · OHIO STATE UNIVERSITY · PI COMBS, COLIN K, DEL MONTE, FEDERICA · 2017 to 2021
$4.0M
Brain-Gut Communication in Alzheimer's DiseaseR01AG048993 · NIA · UNIVERSITY OF NORTH DAKOTA · PI COMBS, COLIN K · 2015 to 2019
$1.4M
APP Regulates Brain and Adipose Changes in ObesityR01AG042819 · NIA · UNIVERSITY OF NORTH DAKOTA · PI COMBS, COLIN K, GOLOVKO, MIKHAIL Y · 2012 to 2016
$1.4M
NIA NIH HHS R01 AG042819NIA NIH HHS R01 AG048993NIA NIH HHS R01 AG057046NIDDK NIH HHS R01 DK040484NIGMS NIH HHS P20 GM113123NIGMS NIH HHS P30 GM103329
6 · The paper itself

Abstract

It is well known that mutations in the gene coding for amyloid precursor protein are responsible for autosomal dominant forms of Alzheimer's disease. Proteolytic processing of the protein leads to a number of metabolites including the amyloid beta peptide. Although brain amyloid precursor protein expression and amyloid beta production are associated with the pathophysiology of Alzheimer's disease, it is clear that amyloid precursor protein is expressed in numerous cell types and tissues. Here we demonstrate that amyloid precursor protein is involved in regulating the phenotype of both adipocytes and peripheral macrophages and is required for high fat diet-dependent weight gain in mice. These data suggest that functions of this protein include modulation of the peripheral immune system and lipid metabolism. This biology may have relevance not only to the pathophysiology of Alzheimer's disease but also diet-associated obesity.

Indexed as

PhenotypeWeight GainAdipose TissueAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBiomarkersDietDiet, High-FatDisease Models, AnimalInflammation MediatorsMacrophagesMaleMiceMice, KnockoutAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBiomarkersInflammation Mediators

Identifiers

PMID28262782
PMCPMC5338020

What OpenQuestion holds

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LicenceCC BY
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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.