Evidence map›Paper›PMID 31816440›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2020

High fat diet consumption results in mitochondrial dysfunction, oxidative stress, and oligodendrocyte loss in the central nervous system.

Monica R Langley, Hyesook Yoon, Ha Neui Kim, Chan-Il Choi, Whitney Simon, Laurel Kleppe, Ian R Lanza, Nathan K LeBrasseur, Aleksey Matveyenko, Isobel A Scarisbrick

Abstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
–field-weighted citation impact
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

51 citing papers in PubMed.

  1. Trial
  2. Effects of obesity on brain health and cognition.Nature reviews. Neurology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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.

Monica R LangleyDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA.
Hyesook YoonDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA.
Ha Neui KimDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA.
Chan-Il ChoiDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA.
Whitney SimonDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA.
Laurel KleppeDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA.
Ian R LanzaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA; Department of Endocrinology, Mayo Clinic, Rochester, MN 55905, USA.
Nathan K LeBrasseurDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA.
Aleksey MatveyenkoDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA; Department of Endocrinology, Mayo Clinic, Rochester, MN 55905, USA.
Isobel A ScarisbrickDepartment of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: scarisbrick.isobel@mayo.edu.

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
TECHNOLOGY NMR SPECTROSCOPYU24DK100469 · NIDDK · MAYO CLINIC ROCHESTER · PI NAIR, K SREEKUMARAN · 2013 to 2017
$9.0M
Role of Protease Activated Receptors in Spinal Cord Injury and RepairR01NS052741 · NINDS · MAYO CLINIC ROCHESTER · PI SCARISBRICK, ISOBEL A · 2008 to 2017
$3.6M
Targeting Protease Activated Receptor 1 for Repair of the Injured Spinal CordR01NS120877 · NINDS · MAYO CLINIC ROCHESTER · PI SCARISBRICK, ISOBEL A · 2021 to 2024
$1.9M
NCATS NIH HHS UL1 TR000135NIDDK NIH HHS U24 DK100469NINDS NIH HHS R01 NS052741NINDS NIH HHS R01 NS120877
6 · The paper itself

Abstract

Metabolic syndrome is a key risk factor and co-morbidity in multiple sclerosis (MS) and other neurological conditions, such that a better understanding of how a high fat diet contributes to oligodendrocyte loss and the capacity for myelin regeneration has the potential to highlight new treatment targets. Results demonstrate that modeling metabolic dysfunction in mice with chronic high fat diet (HFD) consumption promotes loss of oligodendrocyte progenitors across the brain and spinal cord. A number of transcriptomic and metabolomic changes in ER stress, mitochondrial dysfunction, and oxidative stress pathways in HFD-fed mouse spinal cords were also identified. Moreover, deficits in TCA cycle intermediates and mitochondrial respiration were observed in the chronic HFD spinal cord tissue. Oligodendrocytes are known to be particularly vulnerable to oxidative damage, and we observed increased markers of oxidative stress in both the brain and spinal cord of HFD-fed mice. We additionally identified that increased apoptotic cell death signaling is underway in oligodendrocytes from mice chronically fed a HFD. When cultured under high saturated fat conditions, oligodendrocytes decreased both mitochondrial function and differentiation. Overall, our findings show that HFD-related changes in metabolic regulators, decreased mitochondrial function, and oxidative stress contribute to a loss of myelinating cells. These studies identify HFD consumption as a key modifiable lifestyle factor for improved myelin integrity in the adult central nervous system and in addition new tractable metabolic targets for myelin protection and repair strategies.

Indexed as

AnimalsApoptosisCell DifferentiationDiet, High-FatMaleMetabolic SyndromeMiceMice, Inbred C57BLMitochondriaMitochondrial DiseasesObesityOligodendrogliaOxidation-ReductionOxidative StressApoptosisHigh fat dietMitochondriaMyelinOligodendrocyte

Identifiers

PMID31816440
PMCPMC7982965

What OpenQuestion holds

Textmetadata
LicenceTDM
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.