Evidence map›Paper›PMID 26682540›Full record

ArticleCardiovascular diabetology2015

Insulin treatment increases myocardial ceramide accumulation and disrupts cardiometabolic function.

Aimee E Hodson, Trevor S Tippetts, Benjamin T Bikman

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Sphingomyelin as a key negative mediator in atrial fibrillation via lipid profiling analysis and functional identification.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
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  5. Exosomes in Diabetic Wound Healing: Mechanisms, Applications, and Perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
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  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Sphingolipids and their metabolism in physiology and disease.Nature reviews. Molecular cell biology · 2018
    Review
  14. Getting to the heart of the sphingolipid riddle.Current opinion in physiology · 2018
    Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Aimee E HodsonDepartment of Physiology and Developmental Biology, Brigham Young University, 3017 LSB, Provo, UT, 84602, USA. aimhod@gmail.com.
Trevor S TippettsDepartment of Physiology and Developmental Biology, Brigham Young University, 3017 LSB, Provo, UT, 84602, USA. Trevor.Tippetts@utsouthwestern.edu.
Benjamin T BikmanDepartment of Physiology and Developmental Biology, Brigham Young University, 3017 LSB, Provo, UT, 84602, USA. benjamin_bikman@byu.edu.
Brigham Young University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStates of hyperinsulinemia, particularly insulin resistance and type 2 diabetes mellitus, are becoming remarkably common, with roughly half a billion people likely to suffer from the disorder within the next 15 years. Along with this rise has been an associated increased burden of cardiovascular disease. Considering type 2 diabetics treated with insulin are more likely to suffer from heart complications, we sought to determine the specific effect of insulin on ceramide-dependent cardiometabolic risk factors, including insulin resistance and altered heart mitochondrial physiology.

methodsH9c2 cardiomyocytes and adult mice were treated with insulin with or without myriocin to inhibit ceramide biosynthesis. Insulin and glucose changes were tracked throughout the study and mitochondrial bioenergetics was determined in permeabilized cardiomyocytes and myocardium.

resultsHerein, we demonstrate that insulin is sufficient to disrupt heart mitochondrial respiration in both isolated cardiomyocytes and whole myocardium, possibly by increasing mitochondrial fission. Further, insulin increases ceramide accrual in a time-dependent manner, which is necessary for insulin-induced alterations in heart mitochondrial respiration and insulin resistance.

conclusionsCollectively, these observations have two implications. First, they indicate a pathological role of insulin in heart complications stemming from mitochondrial disruption. Second, they identify ceramide as a possible mediator of insulin-related heart disorders.

Indexed as

AnimalsCell LineCell RespirationCeramidesEnergy MetabolismFatty Acids, MonounsaturatedHyperinsulinismHypoglycemic AgentsInsulinInsulin ResistanceMaleMice, Inbred C57BLMitochondria, HeartMyocytes, CardiacRatsTime FactorsCeramidesFatty Acids, MonounsaturatedHypoglycemic AgentsInsulinthermozymocidin

Identifiers

PMID26682540
PMCPMC4683786
OpenAlexW2220030859

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.