Evidence map›Paper›PMID 32816832›Full record

ArticleBMJ open diabetes research & care2020

Expression of clock gene

Kentaro Ushijima, Chisato Suzuki, Hiroko Kitamura, Ken Shimada, Hirotoshi Kawata, Akira Tanaka, Hisanaga Horie, Yoshinori Hosoya, Yasushi Imai, Chikamasa Yamashita and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMJ open diabetes research & care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Kentaro UshijimaDivision of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke, Tochigi, Japan ushijima-kentarou@umin.ac.jp.ORCID 0000-0003-2637-3916
Chisato SuzukiDivision of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Hiroko KitamuraDivision of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Ken ShimadaDivision of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Hirotoshi KawataDivision of Human Pathology, Department of Pathology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Akira TanakaDivision of Human Pathology, Department of Pathology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Hisanaga HorieDivision of Gastroenterological Surgery, Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Yoshinori HosoyaDivision of Gastroenterological Surgery, Department of Surgery, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Yasushi ImaiDivision of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Chikamasa YamashitaDepartment of Pharmaceutics & Drug Delivery Systems, Tokyo University of Science, Noda, Chiba, Japan.
Akio FujimuraDivision of Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Jichi Medical University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionWe previously reported in ob/ob mice, one of animal models of human type 2 diabetes mellitus (DM2), that (i) acetylation of histone H3 lysine 9 (H3K9) at the promoter region of clock gene RESEARCH DESIGN AND

methodsThe present study was undertaken to evaluate whether such the changes in visceral adipose tissue were detected in patients with DM2. We obtained omental and mesenteric adipose tissue during surgery of lymph node dissection for gastric and colorectal cancers, and investigated these variables in adipose tissue (omental from gastric cancer; 13 non-DM, 12 DM2: mesenteric from colorectal cancer; 12 non-DM, 11 DM2).

resultsAcetylation of histone H3K9 at the promoter region of

conclusionsThe changes in DBP-PPAR-γ axis observed in mice with diabetes were also detected in patients with DM2. Because adiponectin secretion is reported to be enhanced through the PPAR-γ-related mechanism, this study supports the hypothesis that omental adipose tissue is involved in the mechanism of DM2.

Indexed as

Diabetes Mellitus, Type 2Adipose TissueDNA-Binding ProteinsGene Expression RegulationHumansPPAR gammaRNA, MessengerTranscription FactorsDBP protein, humanDNA-Binding ProteinsPPAR gammaRNA, MessengerTranscription Factorscircadian rhythmgene expression

Identifiers

PMID32816832
PMCPMC7437886
OpenAlexW3073120040

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.