Evidence map›Paper›PMID 28720899›Full record

ArticleScientific reports2017

p32 heterozygosity protects against age- and diet-induced obesity by increasing energy expenditure.

Yong Liu, Patrick L Leslie, Aiwen Jin, Koji Itahana, Lee M Graves, Yanping Zhang

Open access · goldAbstract 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  11. International journal of biological sciences · 2021
    Article
  12. Article
  13. The Expression Pattern ofInternational journal of molecular sciences · 2019
    Article
  14. p32 regulates ER stress and lipid homeostasis by down-regulating GCS1 expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    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

6 authors at 2 institutions in 3 countries.

Yong LiuDepartment of Radiation Oncology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599-7461, USA.
Patrick L LeslieDepartment of Radiation Oncology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599-7461, USA.
Aiwen JinDepartment of Radiation Oncology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599-7461, USA.
Koji ItahanaDepartment of Radiation Oncology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599-7461, USA.
Lee M GravesDepartment of Pharmacology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599-7461, USA.
Yanping ZhangDepartment of Radiation Oncology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599-7461, USA. ypzhang@med.unc.edu.
University of North Carolina at Chapel Hill · USXuzhou Medical College · CN

Funding

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SUSAN M. SMITH · 1999 to 2026
$31.6M
NRSA IN GENETICST32GM007092 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SEKELSKY, JEFF J. · 1985 to 2019
$5.9M
Mitochondrial p32 regulation of the Mdm2-p53 tumor suppression signaling and apopR01CA155235 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YANPING · 2012 to 2016
$1.5M
NCI NIH HHS R01 CA155235NIDDK NIH HHS P30 DK056350NIGMS NIH HHS T32 GM007092
6 · The paper itself

Abstract

Obesity is increasing in prevalence and has become a global public health problem. The main cause of obesity is a perturbation in energy homeostasis, whereby energy intake exceeds energy expenditure. Although mitochondrial dysfunction has been linked to the deregulation of energy homeostasis, the precise mechanism is poorly understood. Here, we identify mitochondrial p32 (also known as C1QBP) as an important regulator of lipid homeostasis that regulates both aerobic and anaerobic energy metabolism. We show that while whole-body deletion of the p32 results in an embryonic lethal phenotype, mice heterozygous for p32 are resistant to age- and high-fat diet-induced ailments, including obesity, hyperglycemia, and hepatosteatosis. Notably, p32

Indexed as

AnimalsDiet, High-FatEnergy IntakeEnergy MetabolismGlycolysisHeterozygoteHomeostasisHyperglycemiaInsulin ResistanceMice, Inbred C57BLMice, KnockoutMitochondrial ProteinsObesityOxygen ConsumptionC1qbp protein, mouseMitochondrial Proteins

Identifiers

PMID28720899
PMCPMC5516014
OpenAlexW2735334089

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.