Evidence map›Paper›PMID 37561578›Full record

ArticleJCI insight2023

ACOT1 deficiency attenuates high-fat diet-induced fat mass gain by increasing energy expenditure.

Timothy D Heden, Mallory P Franklin, Christina Dailey, Mara T Mashek, Chen Chen, Douglas G Mashek

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. The Physiological and Pathological Role of Acyl-CoA Oxidation.International journal of molecular sciences · 2023
    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

6 authors at 2 institutions in 2 countries.

Timothy D HedenPennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
Mallory P FranklinDepartment of Biochemistry, Molecular Biology and Biophysics and.
Christina DaileyDepartment of Biochemistry, Molecular Biology and Biophysics and.
Mara T MashekDepartment of Biochemistry, Molecular Biology and Biophysics and.
Chen ChenDepartment of Biochemistry, Molecular Biology and Biophysics and.
Douglas G MashekDepartment of Biochemistry, Molecular Biology and Biophysics and.
University of Minnesota · USPennington Biomedical Research Center · US

Funding

The role of maternal obesity-driven inflammation and adverse pregnancy outcomes in a mouse model of preeclampsiaP20GM135002 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Jacqueline M Stephens · 2020 to 2026
$18.4M
Minnesota Obesity Prevention Training (MnOPT)T32DK083250 · NIDDK · UNIVERSITY OF MINNESOTA · PI KOTZ, CATHERINE M, LASKA, MELISSA N. · 2010 to 2024
$5.1M
Regulation and consequences of hepatic lipid droplet catabolismR01DK114401 · NIDDK · UNIVERSITY OF MINNESOTA · PI MASHEK, DOUGLAS G · 2017 to 2020
$1.7M
Role of ATGL and lipid metabolism in healthspanR01AG055452 · NIA · UNIVERSITY OF MINNESOTA · PI MASHEK, DOUGLAS G · 2017 to 2021
$1.6M
Synergistic effects of diet, lipolytic signaling and SIRT1 on energy metabolismR01DK108790 · NIDDK · UNIVERSITY OF MINNESOTA · PI MASHEK, DOUGLAS G · 2016 to 2018
$1.1M
Skeletal muscle mitochondrial phosphatidylethanolamine and respiratorycapacityF32DK109556 · NIDDK · UNIVERSITY OF MINNESOTA · PI HEDEN, TIMOTHY D. · 2016 to 2018
$118k
NIA NIH HHS R01 AG055452NIDDK NIH HHS F32 DK109556NIDDK NIH HHS L30 DK110338NIDDK NIH HHS R01 DK108790NIDDK NIH HHS R01 DK114401NIDDK NIH HHS T32 DK083250NIGMS NIH HHS P20 GM135002
6 · The paper itself

Abstract

Acyl-CoA thioesterase 1 (ACOT1) catalyzes the hydrolysis of long-chain acyl-CoAs to free fatty acids and CoA and is typically upregulated in obesity. Whether targeting ACOT1 in the setting of high-fat diet-induced (HFD-induced) obesity would be metabolically beneficial is not known. Here we report that male and female ACOT1KO mice are partially protected from HFD-induced obesity, an effect associated with increased energy expenditure without alterations in physical activity or food intake. In males, ACOT1 deficiency increased mitochondrial uncoupling protein-2 (UCP2) protein abundance while reducing 4-hydroxynonenal, a marker of oxidative stress, in white adipose tissue and liver of HFD-fed mice. Moreover, concurrent knockdown (KD) of UCP2 with ACOT1 in hepatocytes prevented increases in oxygen consumption observed with ACOT1 KD during high lipid loading, suggesting that UCP2-induced uncoupling may increase energy expenditure to attenuate weight gain. Together, these data indicate that targeting ACOT1 may be effective for obesity prevention during caloric excess by increasing energy expenditure.

Indexed as

Diet, High-FatObesityThiolester HydrolasesAnimalsEnergy MetabolismFemaleLiverMaleMiceWeight GainAcot1 protein, mouseThiolester HydrolasesFatty acid oxidationMetabolismObesityUncoupling proteins

Identifiers

PMID37561578
PMCPMC10561717
OpenAlexW4385737616

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.