Evidence map›Paper›PMID 25760036›Full record

ArticlePloS one2015

Metabolic and tissue-specific regulation of acyl-CoA metabolism.

Jessica M Ellis, Caitlyn E Bowman, Michael J Wolfgang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 116 citations in OpenAlex.

  1. AnGenes · 2026
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5 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

3 authors at 2 institutions in 1 country.

Jessica M EllisDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Center for Metabolism and Obesity Research, Baltimore, Maryland 21205 United States of America.
Caitlyn E BowmanDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Center for Metabolism and Obesity Research, Baltimore, Maryland 21205 United States of America.
Michael J WolfgangDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Center for Metabolism and Obesity Research, Baltimore, Maryland 21205 United States of America.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
Diabetes Research and Training CenterP60DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WONDISFORD, FREDRIC E. · 2008 to 2012
$9.1M
Regulation of Neuronal Lipid Homeostasis By ThioesterasesR01NS072241 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WOLFGANG, MICHAEL J. · 2011 to 2020
$4.0M
NIDDK NIH HHS P60 DK079637NIDDK NIH HHS P60DK079637NIGMS NIH HHS T32 GM007445NINDS NIH HHS NS072241NINDS NIH HHS R01 NS072241
6 · The paper itself

Abstract

Acyl-CoA formation initiates cellular fatty acid metabolism. Acyl-CoAs are generated by the ligation of a fatty acid to Coenzyme A mediated by a large family of acyl-CoA synthetases (ACS). Conversely, acyl-CoAs can be hydrolyzed by a family of acyl-CoA thioesterases (ACOT). Here, we have determined the transcriptional regulation of all ACS and ACOT enzymes across tissues and in response to metabolic perturbations. We find patterns of coordinated regulation within and between these gene families as well as distinct regulation occurring in a tissue- and physiologically-dependent manner. Due to observed changes in long-chain ACOT mRNA and protein abundance in liver and adipose tissue, we determined the consequence of increasing cytosolic long-chain thioesterase activity on fatty acid metabolism in these tissues by generating transgenic mice overexpressing a hyperactive mutant of Acot7 in the liver or adipose tissue. Doubling cytosolic acyl-CoA thioesterase activity failed to protect mice from diet-induced obesity, fatty liver or insulin resistance, however, overexpression of Acot7 in adipocytes rendered mice cold intolerant. Together, these data suggest distinct modes of regulation of the ACS and ACOT enzymes and that these enzymes act in a coordinated fashion to control fatty acid metabolism in a tissue-dependent manner.

Indexed as

Acyl Coenzyme AAdipose TissueAnimalsCoenzyme A LigasesGene Expression Regulation, EnzymologicLipid MetabolismLiverMaleMiceMice, Inbred C57BLMice, TransgenicOrgan SpecificityPalmitoyl-CoA HydrolaseAcot7 protein, mouseAcyl Coenzyme ACoenzyme A LigasesPalmitoyl-CoA Hydrolase

Identifiers

PMID25760036
PMCPMC4356623
OpenAlexW1974020172

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.