Evidence map›Paper›PMID 31719103›Full record

ArticleJournal of lipid research2020

Glucometabolic consequences of acute and prolonged inhibition of fatty acid oxidation.

Anne-Marie Lundsgaard, Andreas M Fritzen, Trine S Nicolaisen, Christian S Carl, Kim A Sjøberg, Steffen H Raun, Anders B Klein, Eva Sanchez-Quant, Jakob Langer, Cathrine Ørskov and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.4field-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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Mechanisms of Myocardial Damage Due to Hyperlipidemia: A Review of Recent Studies.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Enhancing Fatty Acids OxidationFrontiers in pharmacology · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Oral GLP1 Analog: Where Does the Tide Go?Clinical medicine insights. Endocrinology and diabetes · 2020
    Review
  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

15 authors at 2 institutions in 2 countries.

Anne-Marie LundsgaardSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Andreas M FritzenSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Trine S NicolaisenSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Christian S CarlSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Kim A SjøbergSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Steffen H RaunSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Anders B KleinNovo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Eva Sanchez-QuantInstitute for Diabetes and Obesity, Helmholtz Diabetes Center at Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany.
Jakob LangerInstitute for Diabetes and Obesity, Helmholtz Diabetes Center at Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany.
Cathrine ØrskovDepartment of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Christoffer ClemmensenNovo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Matthias H TschöpInstitute for Diabetes and Obesity, Helmholtz Diabetes Center at Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; German Center for Diabetes Research (DZD), Helmholtz Zentrum München, Neuherberg, Germany; Division of Metabolic Diseases, Technische Universität München, München, Germany.
Erik A RichterSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Bente KiensSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark. Electronic address: bkiens@nexs.ku.dk.
Maximilian KleinertSection of Molecular Physiology, Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark; Institute for Diabetes and Obesity, Helmholtz Diabetes Center at Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. Electronic address: mkleinert@nexs.ku.dk.
University of Copenhagen · DKHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive circulating FAs have been proposed to promote insulin resistance (IR) of glucose metabolism by increasing the oxidation of FAs over glucose. Therefore, inhibition of FA oxidation (FAOX) has been suggested to ameliorate IR. However, prolonged inhibition of FAOX would presumably cause lipid accumulation and thereby promote lipotoxicity. To understand the glycemic consequences of acute and prolonged FAOX inhibition, we treated mice with the carnitine palmitoyltransferase 1 (CPT-1) inhibitor, etomoxir (eto), in combination with short-term 45% high fat diet feeding to increase FA availability. Eto acutely increased glucose oxidation and peripheral glucose disposal, and lowered circulating glucose, but this was associated with increased circulating FAs and triacylglycerol accumulation in the liver and heart within hours. Several days of FAOX inhibition by daily eto administration induced hepatic steatosis and glucose intolerance, specific to CPT-1 inhibition by eto. Lower whole-body insulin sensitivity was accompanied by reduction in brown adipose tissue (BAT) uncoupling protein 1 (UCP1) protein content, diminished BAT glucose clearance, and increased hepatic glucose production. Collectively, these data suggest that pharmacological inhibition of FAOX is not a viable strategy to treat IR, and that sufficient rates of FAOX are required for maintaining liver and BAT metabolic function.

Indexed as

AnimalsDiet, High-FatEpoxy CompoundsFatty AcidsGlucoseGlucose IntoleranceMaleMiceMice, Inbred C57BLOxidation-ReductionEpoxy CompoundsetomoxirFatty AcidsGlucosebrown adipose tissuecarnitine palmitoyltransferase 1hepatic glucose productionhyperglycemiainsulin resistancelipotoxicitylivermitochondrial long-chain fatty acid import

Identifiers

PMID31719103
PMCPMC6939602
OpenAlexW2983396554

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.