Evidence map›Paper›PMID 15096593›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Stearoyl-CoA desaturase 1 deficiency increases fatty acid oxidation by activating AMP-activated protein kinase in liver.

Pawel Dobrzyn, Agnieszka Dobrzyn, Makoto Miyazaki, Paul Cohen, Esra Asilmaz, D Grahame Hardie, Jeffrey M Friedman, James M Ntambi

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

179 citing papers in PubMed, 398 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Enhanced fatty acid oxidation via SCD1 downregulation fuels cardiac reprogramming.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  11. Review
  12. Therapeutic Strategies for MASH: An Update on Drug Candidates Under Investigation in Late-Phase Clinical Trials.International journal of translational medicine (Basel, Switzerland) · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

119 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

8 authors at 4 institutions in 2 countries.

Pawel DobrzynDepartment of Biochemistry, University of Wisconsin, Madison, WI 53706, USA.
Agnieszka Dobrzyn
Makoto Miyazaki
Paul Cohen
Esra Asilmaz
D Grahame Hardie
Jeffrey M Friedman
James M Ntambi
Rockefeller University · USUniversity of Wisconsin–Madison · USHoward Hughes Medical Institute · USLaboratory of Molecular Genetics · PL

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
THE GENOMIC BASIS OF HERITABLE OBESITY IN MICER01DK041096 · NIDDK · ROCKEFELLER UNIVERSITY · PI FRIEDMAN, JEFFREY M · 1989 to 2013
$4.9M
Role of Stearoyl-CoA Desaturase in MetabolismR01DK062388 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI NTAMBI, JAMES M. · 2002 to 2010
$2.6M
NIDDK NIH HHS R01 DK041096NIDDK NIH HHS R01 DK062388NIDDK NIH HHS R01-DK41096NIDDK NIH HHS R01-DK62388NIGMS NIH HHS T32 GM007739Wellcome Trust
6 · The paper itself

Abstract

Stearoyl-CoA desaturase (SCD) catalyzes the rate-limiting step in the biosynthesis of monounsaturated fatty acids. Mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased energy expenditure, and up-regulated expression of several genes encoding enzymes of fatty acid beta-oxidation in liver. The mechanisms by which SCD deficiency leads to these metabolic changes are presently unknown. Here we show that the phosphorylation and activity of AMP-activated protein kinase (AMPK), a metabolic sensor that regulates lipid metabolism during increased energy expenditure is significantly increased (approximately 40%, P < 0.01) in liver of SCD1 knockout mice (SCD1-/-). In parallel with the activation of AMPK, the phosphorylation of acetyl-CoA carboxylase at Ser-79 was increased and enzymatic activity was decreased (approximately 35%, P < 0.001), resulting in decreased intracellular levels of malonyl-CoA (approximately 47%, P < 0.001). An SCD1 mutation also increased AMPK phosphorylation and activity and increased acetyl-CoA carboxylase phosphorylation in leptin-deficient ob/ob mice. Lower malonyl-CoA concentrations are known to derepress carnitine palmitoyltransferase 1 (CPT1). In SCD1-/- mice, CPT1 and CPT2 activities were significantly increased (in both cases approximately 60%, P < 0.001) thereby stimulating the oxidation of mitochondrial palmitoyl-CoA. Our results identify AMPK as a mediator of increased fatty acid oxidation in liver of SCD1-deficient mice.

Indexed as

AMP-Activated Protein KinasesAnimalsFatty AcidsLiverMiceMice, KnockoutMultienzyme ComplexesPhosphorylationProtein Serine-Threonine KinasesStearoyl-CoA DesaturaseAMP-Activated Protein KinasesFatty AcidsMultienzyme ComplexesProtein Serine-Threonine KinasesStearoyl-CoA Desaturase

Identifiers

PMID15096593
PMCPMC404058
OpenAlexW2164514101

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.