Evidence map›Paper›PMID 31890673›Full record

ArticleJournal of diabetes and metabolic disorders2019

Integrated analysis of gene modulation profile identifies pathogenic factors and pathways in the liver of diabetic mice.

Thai Quoc Tran, Yuan-Man Hsu, Yu-Chuen Huang, Chao-Jung Chen, Wei-De Lin, Ying-Ju Lin, Wen-Ling Liao, Wei-Yong Lin, Jai-Sing Yang, Jinn-Chyuan Sheu and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of diabetes and metabolic disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

12 authors at 2 institutions in 1 country.

Thai Quoc Tran1Graduate Institute of Biomedical Science, China Medical University, Taichung, 404 Taiwan.
Yuan-Man Hsu2Department of Biological Science and Technology, China Medical University, Taichung, 404 Taiwan.
Yu-Chuen Huang3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
Chao-Jung Chen3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
Wei-De Lin3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
Ying-Ju Lin3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
Wen-Ling Liao3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
Wei-Yong Lin3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
Jai-Sing Yang3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
Jinn-Chyuan Sheu5Institute of Biomedical Science, National Sun Yat-sen University, Kaohsiung, 80424 Taiwan.
Shih-Yin Chen3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.ORCID 0000-0002-6925-7627
Fuu-Jen Tsai3Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404 Taiwan.
China Medical University · TWNational Sun Yat-sen University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeType-2 diabetes mellitus (T2D) is a metabolic disorder that can progress to a serious chronic disease and frequently develops in obese individuals in association with various pathogenic complications that shorten the lifespan of these patients. The liver is an important organ regulating lipid metabolism, which is damaged in both obesity and T2D; however, the specific pathways involved in these pathogenic effects remain unclear. Establishing a suitable animal model that effectively mimics the human biological condition is a critical factor to allow for precise identification of T2D-related genes.

methodsThe KK.Cg-A

resultsWe found that inflammation accompanied by abnormal lipid metabolism led to the spontaneous mechanism of obesity-induced diabetes, resulting in differential expression of some genes related to the terms of insulin resistance and glucose tolerance. Surprisingly, disruption of steroid biosynthesis strongly facilitated the diabetic pathogenesis. To support these findings, we highlighted some candidate genes and determined their relationships in biological networks of obesity-induced T2D.

conclusionThese findings provide valuable reference data that can facilitate further detailed investigations to elucidate the pathogenic mechanism of obesity-induced diabetes in mice, which can be associated with the human condition to inform new prevention and treatment strategies.

Indexed as

KK.Cg-Ay/J mouseLiver metabolismMicroarray analysisObesityType-2 diabetes

Identifiers

PMID31890673
PMCPMC6915200
OpenAlexW2984346829

What OpenQuestion holds

Textmetadata
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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.