Evidence map›Paper›PMID 23328129›Full record

ArticleDiabetes2013

Mitochondrial function in diabetes: novel methodology and new insight.

Liping Yu, Brian D Fink, Judith A Herlein, William I Sivitz

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Evidence for metabolic aberrations in asymptomatic persons with type 2 diabetes after initiation of simvastatin therapy.Translational research : the journal of laboratory and clinical medicine · 2015
    Trial
  3. Review
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  13. Modulation of complex II-energized respiration in muscle, heart, and brown adipose mitochondria by oxaloacetate and complex I electron flow.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Liping YuNMR Core Facility and Department of Biochemistry, University of Iowa, Iowa City, Iowa, USA.
Brian D Fink
Judith A Herlein
William I Sivitz
University of Iowa · US

Funding

Mitochondrial respiratory uncoupling and the pathogenes*R01HL073166 · NHLBI · UNIVERSITY OF IOWA · PI SIVITZ, WILLIAM IRVING · 2003 to 2006
$877k
Mitochondrial-targeted CoQ: Metabolic and Redox Effects and role in DiabetesI01BX000285 · VA · IOWA CITY VA MEDICAL CENTER · PI SIVITZ, WILLIAM IRVING · 2011 to 2017
–
BLRD VA I01 BX000285NHLBI NIH HHS 5R01HL073166NHLBI NIH HHS R01 HL073166
6 · The paper itself

Abstract

Interpreting mitochondrial function as affected by comparative physiologic conditions is confounding because individual functional parameters are interdependent. Here, we studied muscle mitochondrial function in insulin-deficient diabetes using a novel, highly sensitive, and specific method to quantify ATP production simultaneously with reactive oxygen species (ROS) at clamped levels of inner mitochondrial membrane potential (ΔΨ), enabling more detailed study. We used a 2-deoxyglucose (2DOG) energy clamp to set ΔΨ at fixed levels and to quantify ATP production as 2DOG conversion to 2DOG-phosphate measured by one-dimensional (1)H and two-dimensional (1)H/(13)C heteronuclear single quantum coherence nuclear magnetic resonance spectroscopy. These techniques proved far more sensitive than conventional (31)P nuclear magnetic resonance and allowed high-throughput study of small mitochondrial isolates. Over conditions ranging from state 4 to state 3 respiration, ATP production was lower and ROS per unit of ATP generated was greater in mitochondria isolated from diabetic muscle. Moreover, ROS began to increase at a lower threshold for inner membrane potential in diabetic mitochondria. Further, ATP production in diabetic mitochondria is limited not only by respiration but also by limited capacity to use ΔΨ for ATP synthesis. In summary, we describe novel methodology for measuring ATP and provide new mechanistic insight into the dysregulation of ATP production and ROS in mitochondria of insulin-deficient rodents.

Indexed as

Adenosine TriphosphateAnimalsDiabetes MellitusHydrogen PeroxideMagnetic Resonance SpectroscopyMaleMembrane Potential, MitochondrialMitochondriaRatsRats, Sprague-DawleyReactive Oxygen SpeciesAdenosine TriphosphateHydrogen PeroxideReactive Oxygen Species

Identifiers

PMID23328129
PMCPMC3661643
OpenAlexW2124257762

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.