Evidence map›Paper›PMID 24155240›Full record

ArticleThe Journal of biological chemistry2013

NAT8L (N-acetyltransferase 8-like) accelerates lipid turnover and increases energy expenditure in brown adipocytes.

Ariane R Pessentheiner, Helmut J Pelzmann, Evelyn Walenta, Martina Schweiger, Lukas N Groschner, Wolfgang F Graier, Dagmar Kolb, Kyosuke Uno, Toh Miyazaki, Atsumi Nitta and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

64 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The Emerging Role of N-Acetylaspartate in Cancer.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. The Critical Role of GALNTs-Regulated O-GalNAc Glycosylation in Cancer Malignancy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Much ado about NAA-thing.Nature metabolism · 2025
    Article
  17. Article
  18. Review
  19. Review
  20. Review

4 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

13 authors at 4 institutions in 2 countries.

Ariane R PessentheinerFrom the Institute for Genomics and Bioinformatics, Graz University of Technology, Petergasse 14, 8010 Graz, Austria.
Helmut J Pelzmann
Evelyn Walenta
Martina Schweiger
Lukas N Groschner
Wolfgang F Graier
Dagmar Kolb
Kyosuke Uno
Toh Miyazaki
Atsumi Nitta
Dietmar Rieder
Andreas Prokesch
Juliane G Bogner-Strauss
Graz University of Technology · ATMedical University of Graz · ATInnsbruck Medical University · ATUniversity of Toyama · JP

Funding

Austrian Science Fund FWF P 24143Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

NAT8L (N-acetyltransferase 8-like) catalyzes the formation of N-acetylaspartate (NAA) from acetyl-CoA and aspartate. In the brain, NAA delivers the acetate moiety for synthesis of acetyl-CoA that is further used for fatty acid generation. However, its function in other tissues remained elusive. Here, we show for the first time that Nat8l is highly expressed in adipose tissues and murine and human adipogenic cell lines and is localized in the mitochondria of brown adipocytes. Stable overexpression of Nat8l in immortalized brown adipogenic cells strongly increases glucose incorporation into neutral lipids, accompanied by increased lipolysis, indicating an accelerated lipid turnover. Additionally, mitochondrial mass and number as well as oxygen consumption are elevated upon Nat8l overexpression. Concordantly, expression levels of brown marker genes, such as Prdm16, Cidea, Pgc1α, Pparα, and particularly UCP1, are markedly elevated in these cells. Treatment with a PPARα antagonist indicates that the increase in UCP1 expression and oxygen consumption is PPARα-dependent. Nat8l knockdown in brown adipocytes has no impact on cellular triglyceride content, lipogenesis, or oxygen consumption, but lipolysis and brown marker gene expression are increased; the latter is also observed in BAT of Nat8l-KO mice. Interestingly, the expression of ATP-citrate lyase is increased in Nat8l-silenced adipocytes and BAT of Nat8l-KO mice, indicating a compensatory mechanism to sustain the acetyl-CoA pool once Nat8l levels are reduced. Taken together, our data show that Nat8l impacts on the brown adipogenic phenotype and suggests the existence of the NAT8L-driven NAA metabolism as a novel pathway to provide cytosolic acetyl-CoA for lipid synthesis in adipocytes.

Indexed as

Energy MetabolismLipid MetabolismAcetyl Coenzyme AAcetyltransferasesAdipocytes, BrownAdipogenesisAnimalsCell Cycle ProteinsGene Expression Regulation, EnzymologicGene Knockout TechniquesGene SilencingHumansIon ChannelsKineticsMaleMiceAcetyl Coenzyme AAcetyltransferasesATP-citrate lyase kinaseCell Cycle ProteinsIon ChannelsMicrotubule-Associated ProteinsMitochondrial ProteinsNAT8 protein, humanPhosphoproteinsPPAR alphaProtein KinasesspindlinUCP1 protein, humanUcp1 protein, mouseUncoupling Protein 1Acetyl Coenzyme AAdipose Tissue MetabolismAspartateBrown AdipocytesEnergy ExpenditureFatty Acid MetabolismLipid MetabolismN-AcetylaspartateN-Acetyltransferase 8-like

Identifiers

PMID24155240
PMCPMC3861652
OpenAlexW2074549593

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.