Evidence map›Paper›PMID 35460376›Full record

ArticleActa diabetologica2022

Circulating protein disulfide isomerase family member 4 is associated with type 2 diabetes mellitus, insulin sensitivity, and obesity.

Sheng-Chiang Su, Yi-Jen Hung, Fu-Huang Lin, Chang-Hsun Hsieh, Chieh-Hua Lu, Chu-Yen Chien, Ying-Chen Chen, Peng-Fei Li, Feng-Chih Kuo, Jhih-Syuan Liu and 2 more

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Article in Acta diabetologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 7 citations in OpenAlex.

  1. 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

12 authors at 2 institutions in 1 country.

Sheng-Chiang SuGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.
Yi-Jen HungDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Fu-Huang LinSchool of Public Health, National Defense Medical Center, Taipei, Taiwan, ROC.
Chang-Hsun HsiehDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Chieh-Hua LuDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Chu-Yen ChienGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.
Ying-Chen ChenDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Peng-Fei LiDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Feng-Chih KuoDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Jhih-Syuan LiuDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Nain-Feng ChuDivision of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Sec. 2, Chenggong Rd, Neihu District, Taipei City, 114, Taiwan, ROC.
Chien-Hsing LeeGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC. doc10383@gmail.com.ORCID http://orcid.org/0000-0003-4470-7641
Tri-Service General Hospital · TWNational Defense Medical Center · TW

Funding

Ministry of Science and Technology, Taiwan MOST 105-2314-B-016 -040 -MY3Ministry of Science and Technology, Taiwan MOST 108-2314-B-016 -019 -MY3Ministry of Science and Technology, Taiwan MOST 108-2314-B-016 -033 -MY2Tri-Service General Hospital MAB-105-084Tri-Service General Hospital MAB-108-046Tri-Service General Hospital TSGH-C106-006-S02Tri-Service General Hospital TSGH-C107-006-006-S02Tri-Service General Hospital TSGH-C108-005-006-006-S02Tri-Service General Hospital TSGH-D-110058Tri-Service General Hospital TSGH-D-111115
6 · The paper itself

Abstract

aimsEndoplasmic reticulum (ER) stress is associated with obesity and type 2 diabetes mellitus (T2DM) and increasing evidence demonstrates that some ER stress markers can represent the severity of metabolic dysfunction in either cellular or animal models. However, no appropriate molecule has been identified to demonstrate these relationships in clinical practice.

methodsTo determine whether the serum level of the ER chaperone, protein disulfide isomerase family A, member 4 (PDIA4), is associated with type 2 diabetes mellitus, obesity, and insulin sensitivity, we conducted a cross-sectional study for which a total of 553 adults, including 159 with normal glucose tolerance (NGT), 169 with prediabetes (Pre-DM), and 225 with newly diagnosed T2DM, were recruited.

resultsSerum PDIA4 levels were significantly higher in patients with T2DM than in those with NGT (P < 0.001), even after adjustment for potential confounders. These levels correlated positively with fasting plasma glucose, BMI, waist circumference as well as high-sensitivity C-reactive protein levels, and negatively and strongly correlated with insulin sensitivity. In a multivariate logistic regression analysis, higher serum PDIA4 concentration was observed to be significantly associated with an increased risk of T2DM.

conclusionsOur findings provide new mechanistic insights linking ER stress, T2DM, insulin sensitivity, and obesity, which may, in part, account for the ER chaperone properties associated with PDIA4. The results suggest that PDIA4 may serve as a potential instigator of and a putative therapeutic target for T2DM.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceObesityProtein Disulfide-IsomerasesBlood GlucoseCross-Sectional StudiesFamilyHumansBlood GlucosePDIA4 protein, humanProtein Disulfide-IsomerasesER stressPDIA4T2DM

Identifiers

PMID35460376
OpenAlexW4224321465

What OpenQuestion holds

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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.