Evidence map›Paper›PMID 25301169›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2014

A mitochondrial-targeted coenzyme q analog prevents weight gain and ameliorates hepatic dysfunction in high-fat-fed mice.

Brian D Fink, Judith A Herlein, Deng Fu Guo, Chaitanya Kulkarni, Benjamin J Weidemann, Liping Yu, Justin L Grobe, Kamal Rahmouni, Robert J Kerns, William I Sivitz

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Coenzyme Q10 and Obesity: An Overview.Antioxidants (Basel, Switzerland) · 2025
    Review
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  7. Review
  8. Article
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  16. The role of mitochondrial oxidative stress in the metabolic alterations in diet-induced obesity in rats.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  17. Article
  18. Article
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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 1 institution in 1 country.

Brian D FinkDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Judith A HerleinDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Deng Fu GuoDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Chaitanya KulkarniDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Benjamin J WeidemannDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Liping YuDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Justin L GrobeDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Kamal RahmouniDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
Robert J KernsDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa.
William I SivitzDepartment of Internal Medicine/Endocrinology, University of Iowa and the Iowa City Veterans Affairs Medical Center (B.D.F., J.A.H., W.I.S.), and the Departments of Pharmacology (D.F.G., B.J.W., J.L.G.), Pharmaceutical Sciences and Experimental Therapeutics (C.K., R.J.K.), Biochemistry (L.Y.), Pharmacology and Internal Medicine/Cardiology (K.R.), and Primary Laboratory (W.I.S.), University of Iowa, Iowa City, Iowa william-sivitz@uiowa.edu.
University of Iowa · US

Funding

Role of the brain Renin-Angiotensin Sys. in Cardiovas and Metabolic RegulationP01HL084207 · NHLBI · UNIVERSITY OF IOWA · PI GROBE, JUSTIN L · 2007 to 2022
$30.2M
PREDOCTORAL TRAINING PROGRAM IN BIOTECHNOLOGYT32GM008365 · NIGMS · UNIVERSITY OF IOWA · PI KERNS, ROBERT JOHN · 1990 to 2021
$3.8M
Mitochondrial respiratory uncoupling and the pathogenes*R01HL073166 · NHLBI · UNIVERSITY OF IOWA · PI SIVITZ, WILLIAM IRVING · 2003 to 2006
$877k
Mitochondrial-targeted CoQ: Metabolic and Redox Effects and role in DiabetesI01BX000285 · VA · IOWA CITY VA MEDICAL CENTER · PI SIVITZ, WILLIAM IRVING · 2011 to 2017
–
BLRD VA I01 BX000285NHLBI NIH HHS 5R01-HL073166NHLBI NIH HHS P01 HL084207NHLBI NIH HHS R01 HL073166NIGMS NIH HHS T32 GM008365NIGMS NIH HHS T32-GM008365
6 · The paper itself

Abstract

We hypothesized that the mitochondrial-targeted antioxidant, mitoquinone (mitoQ), known to have mitochondrial uncoupling properties, might prevent the development of obesity and mitigate liver dysfunction by increasing energy expenditure, as opposed to reducing energy intake. We administered mitoQ or vehicle (ethanol) to obesity-prone C57BL/6 mice fed high-fat (HF) or normal-fat (NF) diets. MitoQ (500 µM) or vehicle (ethanol) was added to the drinking water for 28 weeks. MitoQ significantly reduced total body mass and fat mass in the HF-fed mice but had no effect on these parameters in NF mice. Food intake was reduced by mitoQ in the HF-fed but not in the NF-fed mice. Average daily water intake was reduced by mitoQ in both the NF- and HF-fed mice. Hypothalamic expression of neuropeptide Y, agouti-related peptide, and the long form of the leptin receptor were reduced in the HF but not in the NF mice. Hepatic total fat and triglyceride content did not differ between the mitoQ-treated and control HF-fed mice. However, mitoQ markedly reduced hepatic lipid hydroperoxides and reduced circulating alanine aminotransferase, a marker of liver function. MitoQ did not alter whole-body oxygen consumption or liver mitochondrial oxygen utilization, membrane potential, ATP production, or production of reactive oxygen species. In summary, mitoQ added to drinking water mitigated the development of obesity. Contrary to our hypothesis, the mechanism involved decreased energy intake likely mediated at the hypothalamic level. MitoQ also ameliorated HF-induced liver dysfunction by virtue of its antioxidant properties without altering liver fat or mitochondrial bioenergetics.

Indexed as

AnimalsDietary FatsDiet, High-FatLiver DiseasesMaleMiceMice, Inbred C57BLMitochondria, LiverOrganophosphorus CompoundsUbiquinoneWeight GainDietary FatsmitoquinoneOrganophosphorus CompoundsUbiquinone

Identifiers

PMID25301169
PMCPMC4244581
OpenAlexW2127246484

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.