Evidence map›Paper›PMID 28123441›Full record

ArticleHepatitis monthly2016

Liver Mitochondrial DNA Copy Number and Deletion Levels May Contribute to Nonalcoholic Fatty Liver Disease Susceptibility.

Sharareh Kamfar, Seyed Moayed Alavian, Massoud Houshmand, Reza Yadegarazari, Bahram Seifi Zarei, Alireza Khalaj, Noshin Shabab, Massoud Saidijam

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

Article in Hepatitis monthly, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 14% 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, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  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

8 authors at 5 institutions in 1 country.

Sharareh KamfarDepartment of Molecular Medicine and Genetics, School of Medicine, Hamadan University of Medical Sciences, Hamadan, IR Iran; Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, IR Iran.
Seyed Moayed AlavianBaqiyatallah Research Center for Gastroenterology and Liver Diseases (BRCGL), Baqiyatallah University of Medical Sciences, Tehran, IR Iran; Middle East Liver Diseases (MELD) Center, Tehran, IR Iran.
Massoud HoushmandDepartment of Medical Genetics, National Institute for Genetic Engineering and Biotechnology, Tehran, IR Iran.
Reza YadegarazariShohada Hospital of Harsin, Kermanshah University of Medical Sciences, Kermanshah, IR Iran.
Bahram Seifi ZareiSchool of Medicine, Shahid Beheshti Hospital, Hamadan University of Medical Sciences, Hamadan, IR Iran.
Alireza KhalajObesity Treatment Center, Department of Surgery, Shahed University, Tehran, IR Iran.
Noshin ShababResearch Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, IR Iran.
Massoud SaidijamDepartment of Molecular Medicine and Genetics, School of Medicine, Hamadan University of Medical Sciences, Hamadan, IR Iran; Research Center for Molecular Medicine, Hamadan University of Medical Sciences, Hamadan, IR Iran.
Hamedan University of Medical Sciences · IRBaqiyatallah University of Medical Sciences · IRKermanshah University of Medical Sciences · IRNational Institute of Genetic Engineering and Biotechnology · IRShahed University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is growing evidence that deficiencies observed in the mitochondrial DNA (mtDNA) functions could play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). We hypothesized that genetic variations in mtDNA could affect the mitochondrial function and contribute to the NAFLD susceptibility.

objectivesIn this study, the possible association of the mtDNA copy number and 4,977-bp deletion levels with NAFLD susceptibility in a sample of Iranian population was evaluated.

methodsThis case-control study included 43 NAFLD patients and 20 control subjects. Genomic DNA was extracted from fresh liver tissue samples by using a DNA isolation kit. The mtDNA copy number and mtDNA deletion levels were measured by quantitative real-time PCR and multiplex PCR.

resultsThe relative expression of mtDNA copy number was 3.7 fold higher in NAFLD patients than healthy controls (P < 0.0001). The results remained significant after adjustment for age, BMI, and gender (P = 0.02). In addition, the mtDNA copy number was 4.3 (P < 0.0001) and 3.2-fold (P < 0.0001) higher in nonalcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH) patients than healthy controls, respectively. Finally, the results showed that the 4,977-bp deletion is not detected in any of liver tissue samples obtained from the 20 control subjects whereas 8 out of 43 NAFLD patients (18.6%) showed the 4,977 -bp deletion in their liver tissues (P = 0.039).

conclusionsThis study indicated an association between mtDNA content in the liver tissue and NAFLD susceptibility that may be a consequence of compensatory response to the cumulative exposures to oxidative damage.

Indexed as

Copy Number VariationsMitochondrial DNANon-Alcoholic Fatty Liver DiseaseNonalcoholic Steatohepatitis

Identifiers

PMID28123441
PMCPMC5237470
OpenAlexW2555901220

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.