Evidence map›Paper›PMID 27705799›Full record

ArticleCell reports2016

Nat1 Deficiency Is Associated with Mitochondrial Dysfunction and Exercise Intolerance in Mice.

Indumathi Chennamsetty, Michael Coronado, Kévin Contrepois, Mark P Keller, Ivan Carcamo-Orive, John Sandin, Giovanni Fajardo, Andrew J Whittle, Mohsen Fathzadeh, Michael Snyder and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. STX4 Is Indispensable for Mitochondrial Homeostasis in Skeletal Muscle.Journal of cachexia, sarcopenia and muscle · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Investigation on regulation ofFrontiers in pharmacology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

15 authors at 3 institutions in 1 country.

Indumathi ChennamsettyDivision of Cardiovascular Medicine and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michael CoronadoDivision of Cardiology, Department of Pediatrics, Stanford University, Stanford, CA 94305, USA.
Kévin ContrepoisDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Mark P KellerDepartment of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.
Ivan Carcamo-OriveDivision of Cardiovascular Medicine and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
John SandinDivision of Cardiovascular Medicine and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Giovanni FajardoDivision of Cardiology, Department of Pediatrics, Stanford University, Stanford, CA 94305, USA.
Andrew J WhittleDepartment of Psychiatry, Stanford University, Stanford, CA 94305, USA.
Mohsen FathzadehDivision of Cardiovascular Medicine and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michael SnyderDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Gerald ReavenDivision of Cardiovascular Medicine and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Alan D AttieDepartment of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.
Daniel BernsteinDivision of Cardiology, Department of Pediatrics, Stanford University, Stanford, CA 94305, USA.
Thomas QuertermousDivision of Cardiovascular Medicine and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Joshua W KnowlesDivision of Cardiovascular Medicine and Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: knowlej@stanford.edu.
Stanford University · USCardiovascular Institute of the South · USUniversity of Wisconsin–Madison · US

Funding

Identifying the gene networks of insulin resistance: the GENESIPS studyU01HL107388 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS, SCHADT, ERIC E · 2011 to 2015
$8.8M
Longitudinal Multiomics Microbial Profiling in Healthy and Disease IndividualsU54DK102556 · NIDDK · STANFORD UNIVERSITY · PI SNYDER, MICHAEL P., WEINSTOCK, GEORGE M · 2014 to 2015
$7.7M
Mechanism of the Coronary Heart Disease Association at Chromosome 6q23.2R01HL109512 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2011 to 2019
$6.1M
Training in Myocardial Biology at Stanford (TIMBS)T32HL094274 · NHLBI · STANFORD UNIVERSITY · PI Euan A Ashley, Daniel Bernstein · 2010 to 2026
$5.0M
ROLE OF BETA-RECEPTOR SIGNALING IN CARDIOMYOPATHYR01HL061535 · NHLBI · STANFORD UNIVERSITY · PI BERNSTEIN, DANIEL · 2000 to 2010
$3.3M
Molecular Mechanisms of Insulin Resistance Associated LociR01DK107437 · NIDDK · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2019
$2.2M
Identification of causal coronary heart disease variation in smooth muscle cellsR33HL120757 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2018
$1.6M
Beta-adrenergic signaling modulates mitochondrial function and dynamicsR00HL129474 · NHLBI · WHITMAN COLLEGE · PI CORONADO, MICHAEL J. · 2018 to 2020
$747k
Identification of causal coronary heart disease variation in smooth muscle cellsR21HL120757 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2014 to 2015
$434k
Beta-adrenergic signaling modulates mitochondrial function and dynamicsK99HL129474 · NHLBI · STANFORD UNIVERSITY · PI CORONADO, MICHAEL J. · 2015 to 2016
$296k
NHLBI NIH HHS K99 HL129474NHLBI NIH HHS R00 HL129474NHLBI NIH HHS R01 HL061535NHLBI NIH HHS R01 HL109512NHLBI NIH HHS R21 HL120757NHLBI NIH HHS R33 HL120757NHLBI NIH HHS T32 HL094274NHLBI NIH HHS U01 HL107388NIDDK NIH HHS R01 DK107437NIDDK NIH HHS U54 DK102556
6 · The paper itself

Abstract

We recently identified human N-acetyltransferase 2 (NAT2) as an insulin resistance (IR) gene. Here, we examine the cellular mechanism linking NAT2 to IR and find that Nat1 (mouse ortholog of NAT2) is co-regulated with key mitochondrial genes. RNAi-mediated silencing of Nat1 led to mitochondrial dysfunction characterized by increased intracellular reactive oxygen species and mitochondrial fragmentation as well as decreased mitochondrial membrane potential, biogenesis, mass, cellular respiration, and ATP generation. These effects were consistent in 3T3-L1 adipocytes, C2C12 myoblasts, and in tissues from Nat1-deficient mice, including white adipose tissue, heart, and skeletal muscle. Nat1-deficient mice had changes in plasma metabolites and lipids consistent with a decreased ability to utilize fats for energy and a decrease in basal metabolic rate and exercise capacity without altered thermogenesis. Collectively, our results suggest that Nat1 deficiency results in mitochondrial dysfunction, which may constitute a mechanistic link between this gene and IR.

Indexed as

Physical Conditioning, Animal3T3-L1 CellsAdenosine TriphosphateAdipocytesAnimalsArylamine N-AcetyltransferaseInsulin ResistanceIsoenzymesMembrane Potential, MitochondrialMetabolism, Inborn ErrorsMiceMitochondriaMyocardiumReactive Oxygen SpeciesAdenosine TriphosphateArylamine N-AcetyltransferaseIsoenzymesN-acetyltransferase 1Reactive Oxygen Speciesadipose tissuebasal metabolic ratefatty acidsinsulin resistancemitochondriamitochondrial dysfunctionNat1NAT2reactive oxygen species

Identifiers

PMID27705799
PMCPMC5097870
OpenAlexW2529831231

What OpenQuestion holds

Textmetadata
LicenceTDM
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.