Evidence map›Paper›PMID 32446361›Full record

ArticleBiochemical and biophysical research communications2020

Role of mitochondrial acyl-CoA dehydrogenases in the metabolism of dicarboxylic fatty acids.

Sivakama S Bharathi, Yuxun Zhang, Zhenwei Gong, Radhika Muzumdar, Eric S Goetzman

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Metabolic phenotypes of doxorubicin-induced cardiotoxicity among patients with breast cancer.Metabolomics : Official journal of the Metabolomic Society · 2026
    Article
  2. Article
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  4. Odd-Chain Dicarboxylic Acid Feeding Produces a Glutaric Aciduria Type 1-Like Metabolic Signature in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  16. The Mystery of Extramitochondrial Proteins Lysine Succinylation.International journal of molecular sciences · 2021
    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

5 authors at 1 institution in 1 country.

Sivakama S BharathiDepartment of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15224, USA.
Yuxun ZhangDepartment of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15224, USA.
Zhenwei GongDepartment of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15224, USA.
Radhika MuzumdarDepartment of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15224, USA.
Eric S GoetzmanDepartment of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15224, USA. Electronic address: Eric.goetzman@chp.edu.
University of Pittsburgh · US

Funding

Pittsburgh Liver Research CenterP30DK120531 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Gavin E Arteel · 2019 to 2026
$10.9M
Regulation of Peroxisomal Metabolism by Lysine AcylationR01DK090242 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOETZMAN, ERIC S · 2011 to 2024
$5.4M
NIDDK NIH HHS P30 DK120531NIDDK NIH HHS R01 DK090242
6 · The paper itself

Abstract

Dicarboxylic fatty acids, taken as a nutritional supplement or produced endogenously via omega oxidation of monocarboxylic fatty acids, may have therapeutic potential for rare inborn errors of metabolism as well as common metabolic diseases such as type 2 diabetes. Breakdown of dicarboxylic acids yields acetyl-CoA and succinyl-CoA as products, the latter of which is anaplerotic for the TCA cycle. However, little is known about the metabolic pathways responsible for degradation of dicarboxylic acids. Here, we demonstrated with whole-cell fatty acid oxidation assays that both mitochondria and peroxisomes contribute to dicarboxylic acid degradation. Several mitochondrial acyl-CoA dehydrogenases were tested for activity against dicarboxylyl-CoAs. Medium-chain acyl-CoA dehydrogenase (MCAD) exhibited activity with both six and 12 carbon dicarboxylyl-CoAs, and the capacity for dehydrogenation of these substrates was significantly reduced in MCAD knockout mouse liver. However, when dicarboxylic acids were fed to normal mice, the expression of MCAD did not change, while expression of peroxisomal fatty acid oxidation enzymes was greatly upregulated. In conclusion, mitochondrial fatty acid oxidation, and in particular MCAD, contributes to dicarboxylic acid degradation, but feeding dicarboxylic acids induces only the peroxisomal pathway.

Indexed as

Acyl-CoA DehydrogenasesAnimalsDicarboxylic AcidsFatty AcidsMaleMiceMice, KnockoutMitochondriaAcyl-CoA DehydrogenasesDicarboxylic AcidsFatty AcidsAcyl-CoA dehydrogenaseAcyl-CoA oxidaseDicarboxylic fatty acidsFatty acid oxidationMitochondriaPeroxisomes

Identifiers

PMID32446361
PMCPMC7248122
OpenAlexW3022931720

What OpenQuestion holds

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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.