Evidence map›Paper›PMID 21881966›Full record

ArticleMetabolic brain disease2011

Non-alcoholic fatty liver induces insulin resistance and metabolic disorders with development of brain damage and dysfunction.

Doaa A Ghareeb, Hani S Hafez, Hend M Hussien, Nihal F Kabapy

Abstract read
PubMed Publisher
In one paragraph

Article in Metabolic brain disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Review
  7. Nonalcoholic Fatty Liver Disease.Handbook of experimental pharmacology · 2022
    Review
  8. Article
  9. Article
  10. Human coronaviruses in idiopathic Parkinson's disease: Implications of SARS-CoV-2's modulation of the host's transcriptome.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2021
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  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

4 authors at 3 institutions in 2 countries.

Doaa A GhareebDepartment of Biochemistry, Faculty of Science, Alexandria University, Moharm Bek, 21511 Alexandria, Egypt.
Hani S Hafez
Hend M Hussien
Nihal F Kabapy
Alexandria University · EGKing Khaled Hospital · SAPharos University in Alexandria · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study we investigated the effect of the non-alcoholic fatty liver disease (NAFLD) on the alterations in the activity of neurotransmitters catabolizing enzymes and energy catabolising enzymes, prooxidants, endogenous antioxidants and proinflammatory cytokines in brain tissue of NAFLD rats. Rats were intraperitonealy injected with CCl4 solution at a dose of (0.021 mole/Kg, 20 μL, body weight) three times weekly for four weeks. Acetylcholine esterase (AChE), monoamine oxidase (MAO), prooxidant/ antioxidants status, ATPase, lipid profile and glucose level were estimated spectrophotometrically while inflammatory markers; interleukin 6 and tumor necrosis factor alpha (IL6 and TNF-α) and insulin were assessed by ELISA technique. Our results showed that the induced NAFLD and insulin resistance (IR) were accompanied with hyperglycemia and hyperlipidemia and lowered brain glucose level with elevated ATPase activity, prooxidant status (TBARS level, xanthine oxidase and cytochrome 2E1 activities), and inflammatory markers. Through the induction period AChE activity was significantly increased compared to control in blood, liver and brain tissues. Also, MAO activity was significantly increased in both brain and liver tissue but decreased in serum compared with control. These biochemical data were supported with pathophysiological analysis that showed severe neurodegeneration, pyknosis acuolations and cavitations. These observations warrant the reassessment of the conventional concept that the NAFLD with IR progression may induce disturbances in activities of neurotransmitters catabolising enzymes and energy production accompanied with oxidative stress and metabolic disorders, acting as relative risk factors for brain dysfunction and damage with the development of age-associated neurodegenerative diseases such as Alzheimer's disease.

Indexed as

AcetylcholinesteraseAdenosine TriphosphatasesAnimalsBlood GlucoseBrainBrain ChemistryCarbon TetrachlorideDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFatty LiverFemaleHyperglycemiaHyperlipidemiasInsulinInsulin ResistanceInterleukin-6AcetylcholinesteraseAdenosine TriphosphatasesBlood GlucoseCarbon TetrachlorideInsulinInterleukin-6Monoamine OxidaseTumor Necrosis Factor-alpha

Identifiers

PMID21881966
OpenAlexW2074674551

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.