Evidence map›Paper›PMID 31940026›Full record

ArticleBioscience reports2020

HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels.

Changxi Chen, Zhongwei Zhu, Yushan Mao, Yimin Xu, Juan Du, Xiaoping Tang, Hongbao Cao

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Genetic Variations ofRisk management and healthcare policy · 2023
    Article
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  7. Article
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  14. HbAJournal of clinical and translational hepatology · 2021
    Article
  15. Observational
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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

7 authors at 2 institutions in 1 country.

Changxi ChenDepartment of Gastroenterology, Hospital of Zhenhai Refine-Chemical Company, Ningbo, Zhejiang Province 315207, China.
Zhongwei ZhuDepartment of Gastroenterology, Hospital of Zhenhai Refine-Chemical Company, Ningbo, Zhejiang Province 315207, China.
Yushan MaoDepartment of Endocrinology, Affiliated Hospital of Medical College of Ningbo University, Ningbo, Zhejiang Province 315020, China.
Yimin XuDepartment of Gastroenterology, Hospital of Zhenhai Refine-Chemical Company, Ningbo, Zhejiang Province 315207, China.
Juan DuDepartment of Gastroenterology, Hospital of Zhenhai Refine-Chemical Company, Ningbo, Zhejiang Province 315207, China.
Xiaoping TangDepartment of Gastroenterology, Hospital of Zhenhai Refine-Chemical Company, Ningbo, Zhejiang Province 315207, China.
Hongbao CaoDepartment of Psychiatry, First Hospital/First Clinical Medical College of Shanxi Medical University, Taiyuan, Shanxi Province 030001, China.
Ningbo University · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous clinical studies highlighted nonalcoholic fatty liver disease (NAFLD) as a hepatic facet of metabolic syndrome, which progresses toward Type 2 diabetes along with an elevation of HbA1c in the blood. Longitudinal observations were performed in a cohort of 2811 participants with no liver disease at inception. The rate of the conversion into NAFLD was 15.7% (440/2811), with a steady increase in prevalence observed in sub-cohorts with increasing HbA1c levels. Moreover, regression analysis indicated that HbA1c levels serve as the risk factors for NAFLD after multiple adjustments (odds ratio: 1.58, P-value < 0.004). When HbA1c-related molecular networks were investigated using natural language programming algorithms, multiple genetic/small molecular (SM) pathways were highlighted as connectors between the HbA1c levels and the development of NAFLD, including ones for nitric oxide, hypoxia and receptor for advanced glycation end products (RAGE). Our results suggest that increased levels of HbA1c may contribute to the progression of NAFLD either directly, by stimulating RAGE or indirectly, through the promotion of hypoxia and suppression of the release of NO. Further studies are needed to test the impact of HbA1c on the development of the chronic liver disease.

Indexed as

AgedAged, 80 and overBiomarkersChinaDiabetes Mellitus, Type 2FemaleGene Regulatory NetworksGlycated HemoglobinHumansIncidenceLongitudinal StudiesMaleMiddle AgedNitric OxideNon-alcoholic Fatty Liver DiseasePrevalenceAGER protein, humanBiomarkersGlycated Hemoglobinhemoglobin A1c protein, humanNitric OxideReceptor for Advanced Glycation End ProductsHbA1cnon-alcoholic fatty liver diseasepathway analysisRAGE

Identifiers

PMID31940026
PMCPMC6997109
OpenAlexW2998761381

What OpenQuestion holds

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LicenceCC BY
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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.