Evidence map›Paper›PMID 21296886›Full record

ArticleThe Journal of biological chemistry2011

Inactivation of the mitochondrial carrier SLC25A25 (ATP-Mg2+/Pi transporter) reduces physical endurance and metabolic efficiency in mice.

Rea P Anunciado-Koza, Jingying Zhang, Jozef Ukropec, Sudip Bajpeyi, Robert A Koza, Richard C Rogers, William T Cefalu, Randall L Mynatt, Leslie P Kozak

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

62 citing papers in PubMed, 105 citations in OpenAlex.

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  20. Time of day determines postexercise metabolism in mouse adipose tissue.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article

2 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Rea P Anunciado-KozaPennington Biomedical Research Center, Baton Rouge, Louisiana 70808, USA.
Jingying Zhang
Jozef Ukropec
Sudip Bajpeyi
Robert A Koza
Richard C Rogers
William T Cefalu
Randall L Mynatt
Leslie P Kozak
Pennington Biomedical Research Center · US

Funding

Research BaseP30DK072476 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2005 to 2026
$26.5M
MOLECULAR GENETICS OF THERMOGENESISR01HD008431 · NICHD · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI KOZAK, LESLIE PAUL · 1986 to 2007
$2.9M
Molecular Genetics of ThermogenesisR01DK089641 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI MYNATT, RANDALL LEE, YOUNG, MARTIN E · 2010 to 2013
$1.6M
NICHD NIH HHS R01 HD008431NICHD NIH HHS R01-HD008431NIDDK NIH HHS 1P30 DK07246NIDDK NIH HHS P30 DK072476NIDDK NIH HHS R01 DK089641PHS HHS P20-TT021925
6 · The paper itself

Abstract

An ATP-Mg(2+/)P(i) inner mitochondrial membrane solute transporter (SLC25A25), which is induced during adaptation to cold stress in the skeletal muscle of mice with defective UCP1/brown adipose tissue thermogenesis, has been evaluated for its role in metabolic efficiency. SLC25A25 is thought to control ATP homeostasis by functioning as a Ca(2+)-regulated shuttle of ATP-Mg(2+) and P(i) across the inner mitochondrial membrane. Mice with an inactivated Slc25a25 gene have reduced metabolic efficiency as evidenced by enhanced resistance to diet-induced obesity and impaired exercise performance on a treadmill. Mouse embryo fibroblasts from Slc25a25(-/-) mice have reduced Ca(2+) flux across the endoplasmic reticulum, basal mitochondrial respiration, and ATP content. Although Slc25a25(-/-) mice are metabolically inefficient, the source of the inefficiency is not from a primary function in thermogenesis, because Slc25a25(-/-) mice maintain body temperature upon acute exposure to the cold (4 °C). Rather, the role of SLC25A25 in metabolic efficiency is most likely linked to muscle function as evidenced from the physical endurance test of mutant mice on a treadmill. Consequently, in the absence of SLC25A25 the efficiency of ATP production required for skeletal muscle function is diminished with secondary effects on adiposity. However, in the absence of UCP1-based thermogenesis, induction of Slc25a25 in mice with an intact gene may contribute to an alternative thermogenic pathway for the maintenance of body temperature during cold stress.

Indexed as

Adenosine TriphosphateAdiposityAnimalsCalciumCalcium-Binding ProteinsCold-Shock ResponseEmbryo, MammalianEnergy MetabolismFibroblastsIon ChannelsMiceMice, KnockoutMitochondrial ProteinsObesityPhysical Conditioning, AnimalPhysical EnduranceAdenosine TriphosphateCalciumCalcium-Binding ProteinsIon ChannelsMitochondrial ProteinsUcp1 protein, mouseUncoupling Protein 1

Identifiers

PMID21296886
PMCPMC3064218
OpenAlexW1983438848

What OpenQuestion holds

Textmetadata
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.