Evidence map›Paper›PMID 18248603›Full record

ArticleJournal of neurochemistry2008

Brain-specific carnitine palmitoyl-transferase-1c: role in CNS fatty acid metabolism, food intake, and body weight.

Michael J Wolfgang, Seung Hun Cha, David S Millington, Gary Cline, Gerald I Shulman, Akira Suwa, Makoto Asaumi, Takeshi Kurama, Teruhiko Shimokawa, M Daniel Lane

Abstract readComparative Study
In one paragraph

Article in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Loss of ACOT7 potentiates seizures and metabolic dysfunction.American journal of physiology. Endocrinology and metabolism · 2019
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

10 authors at 3 institutions in 2 countries.

Michael J WolfgangDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Seung Hun Cha
David S Millington
Gary Cline
Gerald I Shulman
Akira Suwa
Makoto Asaumi
Takeshi Kurama
Teruhiko Shimokawa
M Daniel Lane
Astellas Pharma (Japan) · JPJohns Hopkins University · USJohns Hopkins Medicine · US

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Coordinating and Bioinformatics Unit for the MMPC/DiaCompU24DK076169 · NIDDK · AUGUSTA UNIVERSITY · PI MCINDOE, RICHARD A. · 2006 to 2018
$42.4M
Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Genetic and Cellular Mechanisms of NAFLD and Hepatic Insulin ResistanceR24DK085638 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2010 to 2014
$6.3M
Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
Howard Hughes Medical InstituteNIDDK NIH HHS P30 DK045735NIDDK NIH HHS P30 DK-45735NIDDK NIH HHS R01 DK040936NIDDK NIH HHS R01 DK-40936NIDDK NIH HHS R24 DK085638NIDDK NIH HHS U24 DK059635NIDDK NIH HHS U24 DK076169NIDDK NIH HHS U24 DK-76169
6 · The paper itself

Abstract

While the brain does not utilize fatty acids as a primary energy source, recent evidence shows that intermediates of fatty acid metabolism serve as hypothalamic sensors of energy status. Increased hypothalamic malonyl-CoA, an intermediate in fatty acid synthesis, is indicative of energy surplus and leads to the suppression of food intake and increased energy expenditure. Malonyl-CoA functions as an inhibitor of carnitine palmitoyl-transferase 1 (CPT1), a mitochondrial outer membrane enzyme that initiates translocation of fatty acids into mitochondria for oxidation. The mammalian brain expresses a unique homologous CPT1, CPT1c, that binds malonyl-CoA tightly but does not support fatty acid oxidation in vivo, in hypothalamic explants or in heterologous cell culture systems. CPT1c knockout (KO) mice under fasted or refed conditions do not exhibit an altered CNS transcriptome of genes known to be involved in fatty acid metabolism. CPT1c KO mice exhibit normal levels of metabolites and of hypothalamic malonyl-CoA and fatty acyl-CoA levels either in the fasted or refed states. However, CPT1c KO mice exhibit decreased food intake and lower body weight than wild-type littermates. In contrast, CPT1c KO mice gain excessive body weight and body fat when fed a high-fat diet while maintaining lower or equivalent food intake. Heterozygous mice display an intermediate phenotype. These findings provide further evidence that CPT1c plays a role in maintaining energy homeostasis, but not through altered fatty acid oxidation.

Indexed as

AnimalsBody WeightBrainCarnitine O-PalmitoyltransferaseCentral Nervous SystemChlorocebus aethiopsCHO CellsCOS CellsCricetinaeCricetulusEatingFatty AcidsFemaleIsoenzymesLipid MetabolismMaleCarnitine O-PalmitoyltransferaseFatty AcidsIsoenzymes

Identifiers

PMID18248603
PMCPMC3888516
OpenAlexW1971481079

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.