Evidence map›Paper›PMID 24312551›Full record

ArticlePloS one2013

Enteric neuropathy can be induced by high fat diet in vivo and palmitic acid exposure in vitro.

Ulrikke Voss, Elin Sand, Björn Olde, Eva Ekblad

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-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

35 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Nutraceuticals and Enteric Glial Cells.Molecules (Basel, Switzerland) · 2021
    Review
  9. Disorders of the enteric nervous system - a holistic view.Nature reviews. Gastroenterology & hepatology · 2021
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Glial ACells · 2020
    Article
  15. Article
  16. Review
  17. Article
  18. Estrogen receptor β controls proliferation of enteric glia and differentiation of neurons in the myenteric plexus after damage.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Ulrikke VossDepartment of Experimental Medical Science, Lund University, Lund, Sweden.
Elin Sand
Björn Olde
Eva Ekblad
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveObese and/or diabetic patients have elevated levels of free fatty acids and increased susceptibility to gastrointestinal symptoms. Since the enteric nervous system is pivotal in regulating gastrointestinal functions alterations or neuropathy in the enteric neurons are suspected to occur in these conditions. Lipid induced intestinal changes, in particular on enteric neurons, were investigated in vitro and in vivo using primary cell culture and a high fat diet (HFD) mouse model.

designMice were fed normal or HFD for 6 months. Intestines were analyzed for neuronal numbers, remodeling and lipid accumulation. Co-cultures of myenteric neurons, glia and muscle cells from rat small intestine, were treated with palmitic acid (PA) (0 - 10(-3) M) and / or oleic acid (OA) (0 - 10(-3) M), with or without modulators of intracellular lipid metabolism. Analyses were by immunocyto- and histochemistry.

resultsHFD caused substantial loss of myenteric neurons, leaving submucous neurons unaffected, and intramuscular lipid accumulation in ileum and colon. PA exposure in vitro resulted in neuronal shrinkage, chromatin condensation and a significant and concentration-dependent decrease in neuronal survival; OA exposure was neuroprotective. Carnitine palmitoyltransferase 1 inhibition, L-carnitine- or alpha lipoic acid supplementation all counteracted PA-induced neuronal loss. PA or OA alone both caused a significant and concentration-dependent loss of muscle cells in vitro. Simultaneous exposure of PA and OA promoted survival of muscle cells and increased intramuscular lipid droplet accumulation. PA exposure transformed glia from a stellate to a rounded phenotype but had no effect on their survival.

conclusionsHFD and PA exposure are detrimental to myenteric neurons. Present results indicate excessive palmitoylcarnitine formation and exhausted L-carnitine stores leading to energy depletion, attenuated acetylcholine synthesis and oxidative stress to be main mechanisms behind PA-induced neuronal loss.High PA exposure is suggested to be a factor in causing diabetic neuropathy and gastrointestinal dysregulation.

Indexed as

AMP-Activated Protein KinasesAnimalsCell ProliferationCell SurvivalCeramidesCoculture TechniquesDiet, High-FatEndoplasmic Reticulum StressEnteric Nervous SystemEnzyme ActivationFemaleIntestine, SmallIntracellular SpaceLipid MetabolismMaleMiceAMP-Activated Protein KinasesCeramidesNeurotoxinsOleic AcidPalmitic AcidPalmitoylcarnitinePeroxisome Proliferator-Activated ReceptorsReactive Oxygen Species

Identifiers

PMID24312551
PMCPMC3849255
OpenAlexW2045044805

What OpenQuestion holds

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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.