Evidence map›Paper›PMID 30257974›Full record

ArticleDiabetes2018

Insulin Resistance and Vulnerability to Cardiac Ischemia.

Tomas Jelenik, Ulrich Flögel, Elisa Álvarez-Hernández, Daniel Scheiber, Elric Zweck, Zhaoping Ding, Maik Rothe, Lucia Mastrototaro, Vivien Kohlhaas, Jörg Kotzka and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Review
  5. Review
  6. Observational
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  17. Article
  18. Mechanism of Obesity-Related Lipotoxicity and Clinical Perspective.Advances in experimental medicine and biology · 2024
    Review
  19. Insulin Resistance, Obesity, and Lipotoxicity.Advances in experimental medicine and biology · 2024
    Review
  20. 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

18 authors at 3 institutions in 1 country.

Tomas JelenikInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.ORCID 0000-0002-2061-1162
Ulrich FlögelDepartment of Molecular Cardiology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Elisa Álvarez-HernándezInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.
Daniel ScheiberInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.
Elric ZweckInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.
Zhaoping DingDepartment of Molecular Cardiology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Maik RotheInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.
Lucia MastrototaroInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.
Vivien KohlhaasInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.
Jörg KotzkaGerman Center for Diabetes Research, München-Neuherberg, Germany.
Birgit KnebelGerman Center for Diabetes Research, München-Neuherberg, Germany.
Dirk Müller-WielandDepartment of Medicine I, University Hospital Aachen, Aachen, Germany.ORCID 0000-0002-8807-6442
Sarah MoellendorfDepartment of Cardiovascular Physiology, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Axel GödeckeDepartment of Cardiovascular Physiology, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Malte KelmDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Ralf WestenfeldDivision of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Michael RodenInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany.ORCID 0000-0001-8200-6382
Julia SzendroediInstitute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany julia.szendroedi@ddz.uni-duesseldorf.de.ORCID 0000-0002-5185-8168
Deutsches Diabetes-Zentrum e.V. · DEHeinrich Heine University Düsseldorf · DEUniversitätsklinikum Aachen · DE

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK040936NIDDK NIH HHS U24 DK059635
6 · The paper itself

Abstract

Hepatic and myocardial ectopic lipid deposition has been associated with insulin resistance (IR) and cardiovascular risk. Lipid overload promotes increased hepatic oxidative capacity, oxidative stress, and impaired mitochondrial efficiency, driving the progression of nonalcoholic fatty liver disease (NAFLD). We hypothesized that higher lipid availability promotes ischemia-induced cardiac dysfunction and decreases myocardial mitochondrial efficiency. Mice with adipose tissue-specific overexpression of sterol element-binding protein 1c as model of lipid overload with combined NAFLD-IR and controls underwent reperfused acute myocardial infarcts (AMIs). Whereas indexes of left ventricle (LV) contraction were similar in both groups at baseline, NAFLD-IR showed severe myocardial dysfunction post-AMI, with prominent LV reshaping and increased end-diastolic and end-systolic volumes. Hearts of NAFLD-IR displayed hypertrophy, steatosis, and IR due to 18:1/18:1-diacylglycerol-mediated protein kinase Cε (PKCε) activation. Myocardial fatty acid-linked respiration and oxidative stress were increased, whereas mitochondrial efficiency was decreased. In humans, decreased myocardial mitochondrial efficiency of ventricle biopsies related to IR and troponin levels, a marker of impaired myocardial integrity. Taken together, increased lipid availability and IR favor susceptibility to ischemia-induced cardiac dysfunction. The diacylglycerol-PKCε pathway and reduced mitochondrial efficiency both caused by myocardial lipotoxicity may contribute to the impaired LV compensation of the noninfarcted region of the myocardium.

Indexed as

AnimalsDisease Models, AnimalHumansInsulin ResistanceMiceMitochondria, HeartMyocardial InfarctionMyocardiumNon-alcoholic Fatty Liver DiseaseOxidative Stress

Identifiers

PMID30257974
PMCPMC6245221
OpenAlexW2892590459

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.