Evidence map›Paper›PMID 32581784›Full record

ArticleFrontiers in pharmacology2020

Irisin Improves Myocardial Performance and Attenuates Insulin Resistance in Spontaneous Mutation (

Jianguo Wang, Yu Tina Zhao, Ling Zhang, Patrycja M Dubielecka, Shougang Zhuang, Gangjian Qin, Yu Eugene Chin, Shouyan Zhang, Ting C Zhao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 21 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

9 authors at 7 institutions in 2 countries.

Jianguo WangDepartment of Surgery, Boston University School of Medicine, Roger Williams Medical Center, Providence, RI, United States.
Yu Tina ZhaoDepartment of Surgery, Boston University School of Medicine, Roger Williams Medical Center, Providence, RI, United States.
Ling ZhangDepartment of Medicine, Rhode Island Hospital, Brown University, Providence, RI, United States.
Patrycja M DubieleckaDepartment of Medicine, Rhode Island Hospital, Brown University, Providence, RI, United States.
Shougang ZhuangDepartment of Medicine, Rhode Island Hospital, Brown University, Providence, RI, United States.
Gangjian QinDepartment of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, AL, United States.
Yu Eugene ChinTranslation Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Shouyan ZhangDepartment of Medicine, Luoyang Central Hospital, Zhengzhuo University, Luoyang, China.
Ting C ZhaoDepartment of Surgery, Boston University School of Medicine, Roger Williams Medical Center, Providence, RI, United States.
Brown University · USBoston University · USLuoyang Central Hospital Affiliated to Zhengzhou University · CNProvidence College · USRoger Williams Medical Center · USShanghai Jiao Tong University · CNUniversity of Alabama at Birmingham · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Histone Deacetylase Inhibition: A Novel Approach to CardioprotectionR01HL089405 · NHLBI · ROGER WILLIAMS MEDICAL CENTER · PI ZHAO, TING C · 2009 to 2020
$3.4M
p38 acetylation: Novel signaling mechanisms and myocardial protectionR01HL115265 · NHLBI · ROGER WILLIAMS MEDICAL CENTER · PI ZHAO, TING C · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL089405NHLBI NIH HHS R01 HL115265NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

backgroundIrisin, a newly identified peptide, is critical to regulating metabolism, thermogenesis, and reducing oxidative stresses. Our recent works demonstrated that irisin protected the heart against myocardial ischemic injury and preserved the function of mitochondria. However, whether irisin preserves myocardial performance and attenuates insulin resistance in type II diabetes remains unknown.

objectiveEffects of irisin on type II diabetes-induced cardiac dysfty unction and insulin resistance in db/db mice were studied. Methods: Homozygous db/db mice (n=5/each group) for spontaneous mutation (

resultsHomozygous db/db mice developed an impairment in insulin sensitivity as indicated by Insulin tolerance test (ITT), glucose tolerance test (GTT) (p<0.05 vs non-irisin treatment), hyperglycemia (p<0.05 vs heterozygous control), and hyperinsulinemia (serum insulin: 0.81 ± 0.065 ng/ml in heterozygous control vs. 8.33 ± 0.69 ng/ml in homozygous db/db control, p<0.0001), which were attenuated by the administration of irisin (serum insulin 8.32 ± 0.68 ng/ml in homozygous db/db control vs 6.56 ± 0.38 ng/ml in homozygous db/db irisin treatment, p<0.0001). Furthermore, as compared to heterozygous control, db/db mice manifested a depression in cardiac performance [ejection fraction (EF): 91.9% ± 0.44 in heterozygous control vs 79.1% ± 2.0 in homozygous db/db control, p< 0.001] in associated myocardial remodeling (cardiac fibrosis 1.89% ± 0.09 in heterozygous control vs. 5.39% ± 0.22 in homozygous db/db control, p<0.001). Notably, the depression of cardiac function in EF (79.2% ± 2.0 homozygous db/db control vs. 88.6% ± 1.9 in homozygous db/db + irisin, p<0.01) and fractional shortening (FS) (42.2% ± 1.8 in homozygous db/db control vs. 53.2% ± 2.7 in homozygous db/db+irisin, p<0.01) and remodeling were markedly attenuated by the administration of irisin. Western blotting shows that irisin treatment prevented an approximate two-fold decrease in p38 phosphorylation and increase in histone deacetylase 4 (HDAC4) in the homozygous db/db myocardium (p<0.05 vs homozygous db/db control).

conclusionIrisin preserves myocardial performance and insulin resistance in db/db mice, which is related to p38 phosphorylation and HDAC reduction.

Indexed as

diabetesinsulin resistanceirisinmyocardial functionp38 and HDAC4

Identifiers

PMID32581784
PMCPMC7283381
OpenAlexW3033305481

What OpenQuestion holds

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LicenceCC BY
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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.