Evidence map›Paper›PMID 27596100›Full record

ArticleBMC medical genetics2016

The role of mitochondrial genomics in patients with non-alcoholic steatohepatitis (NASH).

Rohini Mehta, Kianoush Jeiran, Aaron B Koenig, Munkzhul Otgonsuren, Zachary Goodman, Ancha Baranova, Zobair Younossi

Open access · goldAbstract read
In one paragraph

Article in BMC medical genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Mitochondrial Mutations and Genetic Factors Determining NAFLD Risk.International journal of molecular sciences · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Adipose tissue and the physiologic underpinnings of metabolic disease.Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery · 2018
    Review
  15. Article
  16. Article
  17. 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

7 authors at 2 institutions in 1 country.

Rohini MehtaBetty and Guy Beatty Center for Integrated Research, Inova Fairfax Medical Campus, Falls Church, VA, USA.
Kianoush JeiranCenter for the Study of Chronic Metabolic and Rare Diseases, George Mason University, Fairfax, VA, 22033, USA.
Aaron B KoenigBetty and Guy Beatty Center for Integrated Research, Inova Fairfax Medical Campus, Falls Church, VA, USA.
Munkzhul OtgonsurenBetty and Guy Beatty Center for Integrated Research, Inova Fairfax Medical Campus, Falls Church, VA, USA.
Zachary GoodmanBetty and Guy Beatty Center for Integrated Research, Inova Fairfax Medical Campus, Falls Church, VA, USA.
Ancha BaranovaCenter for the Study of Chronic Metabolic and Rare Diseases, George Mason University, Fairfax, VA, 22033, USA.
Zobair YounossiBetty and Guy Beatty Center for Integrated Research, Inova Fairfax Medical Campus, Falls Church, VA, USA. Zobair.younossi@inova.org.
Inova Fairfax Hospital · USGeorge Mason University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVisceral obesity and metabolic syndrome are commonly associated with non-alcoholic fatty liver disease (NAFLD). The progression of steatosis to NASH depends on a number of metabolic and patient-related factors. The mechanisms of genetic predisposition towards the development of NASH and related fibrosis remain unclear. In this study, our aim was to utilize mitotyping and identify mitochondrial haplotypes that may be associated with NAFLD.

methodsWe examined mitochondrial haplotypes along with patatin-like phospholipase domain containing 3 (PNPLA3) rs738409 genotype to determine their association with NAFLD phenotypes. Whole blood samples were obtained from 341 patients (BMI > 35) undergoing weight reduction surgery after written consent. Liver biopsies were centrally reviewed by a single pathologist based on predetermined pathologic protocol (41.9 % Non-NASH NAFLD, 30.4 % NASH, 27.5 % controls). A 1,122 bp of the mitochondrial control loop was sequenced for each sample and classified into haplogroups.

resultsThe presence of haplogroup L exhibits protection against the development of NASH and pericellular fibrosis. The alleles of PNPLA3 locus showed differential distribution in cohorts with NAFLD, NASH and pericellular fibrosis. Heterozygosity at this locus is independently associated with higher risk of having NASH and pericellular fibrosis.

conclusionMitochondrial genetics play an important role in NASH probably by modulation of oxidative stress and the efficiency of oxidative phosphorylation.

Indexed as

Genome, MitochondrialPolymorphism, Single NucleotideAcyltransferasesAdultBiopsyFemaleGenetic Predisposition to DiseaseGenomicsHaplotypesHumansLipaseLiverMaleMembrane ProteinsMiddle AgedMitochondriaAcyltransferasesLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanEthnicityHepatic fibrosisObesityPNPLA3 rs738409

Identifiers

PMID27596100
PMCPMC5011877
OpenAlexW2512006167

What OpenQuestion holds

Textmetadata
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.