Evidence map›Paper›PMID 24696842›Full record

ArticleBioMed research international2014

GCK gene-body hypomethylation is associated with the risk of coronary heart disease.

Limin Xu, Dawei Zheng, Lingyan Wang, Danjie Jiang, Haibo Liu, Leiting Xu, Qi Liao, Lina Zhang, Panpan Liu, Xinbao Shi and 9 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.4field-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

16 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  8. Experimental and therapeutic medicine · 2017
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  12. Oncology letters · 2016
    Article
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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

19 authors at 3 institutions in 1 country.

Limin XuZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; Ningbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Dawei ZhengNingbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Lingyan WangBank of Blood Products, Ningbo No. 2 Hospital, Ningbo, Zhejiang 315010, China.
Danjie JiangZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Haibo LiuYinzhou People's Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315040, China.
Leiting XuZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Qi LiaoZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Lina ZhangZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Panpan LiuZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Xinbao ShiNingbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Zhaoyang WangNingbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Lebo SunNingbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Qingyun ZhouNingbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Ni LiNingbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Yi HuangZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Yanping LeZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Meng YeThe Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.
Guofeng ShaoNingbo Medical Center Lihuili Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315041, China.
Shiwei DuanZhejiang Provincial Key Laboratory of Pathophysiology, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China ; The Affiliated Hospital, Ningbo University School of Medicine, Ningbo, Zhejiang 315211, China.ORCID 0000-0001-7682-2877
Ningbo University · CNNingbo No. 2 Hospital · CNNingbo University Affiliated Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesGlucokinase encoded by GCK is a key enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate. Variants of GCK gene were shown to be associated with type 2 diabetes (T2D) and coronary heart disease (CHD). The goal of this study was to investigate the contribution of GCK gene-body methylation to the risk of CHD. DESIGN AND

methods36 patients (18 males and 18 females) and 36 age- and sex-matched controls were collected for the current methylation research. DNA methylation level of the CpG island (CGI) region on the GCK gene-body was measured through the sodium bisulfite DNA conversion and pyrosequencing technology.

resultsOur results indicated that CHD cases have a much lower methylation level (49.77 ± 6.43%) compared with controls (54.47 ± 7.65%, P = 0.018). In addition, GCK gene-body methylation was found to be positively associated with aging in controls (r = 0.443, P = 0.010).

conclusionsOur study indicated that the hypomethylation of GCK gene-body was significantly associated with the risk of CHD. Aging correlates with an elevation of GCK methylation in healthy controls.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseCase-Control StudiesCoronary DiseaseCpG IslandsDNA MethylationFemaleGlucokinaseHumansMaleRisk FactorsGlucokinase

Identifiers

PMID24696842
PMCPMC3947703
OpenAlexW2058461737

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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.