Evidence map›Paper›PMID 27257426›Full record

ArticleHepatitis monthly2016

Leptin Receptor Gene Polymorphisms and the Risk of Non-Alcoholic Fatty Liver Disease and Coronary Atherosclerosis in the Chinese Han Population.

Bai-Quan An, Lin-Lin Lu, Chen Yuan, Yong-Ning Xin, Shi-Ying Xuan

Open access · hybridAbstract read
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 13 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 3 pooled it
2.2field-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

13 citing papers in PubMed, 3 syntheses or guidelines pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Correlation Between Adiponectin Gene rs1501299 Polymorphism and Nonalcoholic Fatty Liver Disease Susceptibility: A Systematic Review and Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Pooled it
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  13. Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions.International journal of molecular sciences · 2017
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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

5 authors at 3 institutions in 1 country.

Bai-Quan AnDepartment of Gastroenterology, Qingdao Municipal College, Nanjing Medical University, Qingdao, Shandong Province, China.
Lin-Lin LuDigestive Disease Key Laboratory of Qingdao, Qingdao, China; Central Laboratories, Qingdao Municipal Hospital, Qingdao, China.
Chen YuanDepartment of Gastroenterology, Qingdao Municipal College, Nanjing Medical University, Qingdao, Shandong Province, China.
Yong-Ning XinDepartment of Gastroenterology, Qingdao Municipal College, Nanjing Medical University, Qingdao, Shandong Province, China; Digestive Disease Key Laboratory of Qingdao, Qingdao, China; Department of Gastroenterology, Qingdao Municipal Hospital, Qingdao, China.
Shi-Ying XuanDepartment of Gastroenterology, Qingdao Municipal College, Nanjing Medical University, Qingdao, Shandong Province, China; Digestive Disease Key Laboratory of Qingdao, Qingdao, China; Department of Gastroenterology, Qingdao Municipal Hospital, Qingdao, China.
Qingdao Municipal Hospital · CNNanjing Medical University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLeptin receptor (LEPR) polymorphisms have been reported to be associated with lipid metabolism and insulin resistance in various populations. However, whether LEPR polymorphisms are associated with the risks of non-alcoholic fatty liver disease (NAFLD) and coronary atherosclerosis in the Chinese Han population remains unknown.

objectivesTo investigate the association of LEPR polymorphisms at Q223R and K109R with the risks of NAFLD and coronary atherosclerosis in the Chinese Han population. PATIENTS AND

methodsGenotypes of LEPR Q223R and K109R were determined by polymerase chain reaction followed by sequencing in patients with NAFLD (n = 554), coronary atherosclerosis (n = 421), and healthy controls (n = 550). Serum lipid profiles were determined using biochemical methods. Pearson's χ(2) test was used to check for Hardy-Weinberg equilibrium and to analyze the distributions of genotypes' alleles between groups. Baseline characteristics were analyzed using student's t-test, paired-samples t-test, or the χ(2) test where appropriate.

resultsThe LEPR Q223R A allele significantly reduced the risks of both NAFLD and coronary atherosclerosis (OR = 0.683, 95% CI: 0.527 - 0.884, P = 0.004 and OR = 0.724, 95% CI: 0.548 - 0.955, P = 0.022, respectively). Compared to controls, no significant differences in the genotype and allele frequencies of K109R were found in the NAFLD and coronary atherosclerosis populations, respectively. However, there was a significantly increased risk of coronary atherosclerosis in NAFLD patients who carried the K109R A allele (OR = 2.283, 95% CI: 1.556 - 3.348, P < 0.001).

conclusionsLEPR Q223R polymorphisms may confer a significant risk of NAFLD and coronary atherosclerosis. The A allele in the K109R polymorphism might be considered an independent risk factor for coronary atherosclerosis in NAFLD patients.

Indexed as

Coronary AtherosclerosisLEPRNon-Alcoholic Fatty Liver DiseaseSingle Nucleotide Polymorphism

Identifiers

PMID27257426
PMCPMC4888499
OpenAlexW2335056394

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.