Evidence map›Paper›PMID 19542201›Full record

ArticleDiabetes2009

Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice.

Heiko Bugger, Dong Chen, Christian Riehle, Jamie Soto, Heather A Theobald, Xiao X Hu, Balasubramanian Ganesan, Bart C Weimer, E Dale Abel

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

101 citing papers in PubMed, 177 citations in OpenAlex.

  1. Review
  2. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Review
  4. Review
  5. Hypoxia Attenuates Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2024
    Article
  6. TFAM and Mitochondrial Protection in Diabetic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023
    Review
  13. Article
  14. Vitamin A preserves cardiac energetic gene expression in a murine model of diet-induced obesity.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  15. Guidelines on models of diabetic heart disease.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Insulin signaling in the heart.American journal of physiology. Endocrinology and metabolism · 2021
    Review

41 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Heiko BuggerDivision of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Dong Chen
Christian Riehle
Jamie Soto
Heather A Theobald
Xiao X Hu
Balasubramanian Ganesan
Bart C Weimer
E Dale Abel
University of Utah · USUtah State University · US

Funding

ANIMAL MODELS OF DIABETIC CARDIOVASCULAR COMPLICATIONSU01HL070525 · NHLBI · UNIVERSITY OF UTAH · PI MCCLAIN, DONALD A · 2001 to 2005
$3.7M
Modeling Diabetic Cardiomyopathy and Microangiopathy U01HL087947 · NHLBI · UNIVERSITY OF UTAH · PI ABEL, E DALE · 2006 to 2010
$1.8M
NHLBI NIH HHS U01 HL070525NHLBI NIH HHS U01 HL087947NHLBI NIH HHS U01HL087947NHLBI NIH HHS U01HL70525
6 · The paper itself

Abstract

objectiveTo elucidate the molecular basis for mitochondrial dysfunction, which has been implicated in the pathogenesis of diabetes complications. RESEARCH DESIGN AND

methodsMitochondrial matrix and membrane fractions were generated from liver, brain, heart, and kidney of wild-type and type 1 diabetic Akita mice. Comparative proteomics was performed using label-free proteome expression analysis. Mitochondrial state 3 respirations and ATP synthesis were measured, and mitochondrial morphology was evaluated by electron microscopy. Expression of genes that regulate mitochondrial biogenesis, substrate utilization, and oxidative phosphorylation (OXPHOS) were determined.

resultsIn diabetic mice, fatty acid oxidation (FAO) proteins were less abundant in liver mitochondria, whereas FAO protein content was induced in mitochondria from all other tissues. Kidney mitochondria showed coordinate induction of tricarboxylic acid (TCA) cycle enzymes, whereas TCA cycle proteins were repressed in cardiac mitochondria. Levels of OXPHOS subunits were coordinately increased in liver mitochondria, whereas mitochondria of other tissues were unaffected. Mitochondrial respiration, ATP synthesis, and morphology were unaffected in liver and kidney mitochondria. In contrast, state 3 respirations, ATP synthesis, and mitochondrial cristae density were decreased in cardiac mitochondria and were accompanied by coordinate repression of OXPHOS and peroxisome proliferator-activated receptor (PPAR)-gamma coactivator (PGC)-1alpha transcripts.

conclusionsType 1 diabetes causes tissue-specific remodeling of the mitochondrial proteome. Preservation of mitochondrial function in kidney, brain, and liver, versus mitochondrial dysfunction in the heart, supports a central role for mitochondrial dysfunction in diabetic cardiomyopathy.

Indexed as

Adenosine TriphosphateAnimalsBrainCell RespirationDiabetes ComplicationsDiabetes Mellitus, Type 1Fatty AcidsGene Expression ProfilingKidneyLiverMaleMiceMice, Inbred C57BLMice, Mutant StrainsMicroscopy, ElectronMitochondrial DiseasesAdenosine TriphosphateFatty AcidsProteome

Identifiers

PMID19542201
PMCPMC2731527
OpenAlexW2102147313

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.