Evidence map›Paper›PMID 24344248›Full record

ArticleThe Journal of general physiology2014

Sarcolemmal ATP-sensitive potassium channels modulate skeletal muscle function under low-intensity workloads.

Zhiyong Zhu, Ana Sierra, Colin M-L Burnett, Biyi Chen, Ekaterina Subbotina, Siva Rama Krishna Koganti, Zhan Gao, Yuejin Wu, Mark E Anderson, Long-Sheng Song and 4 more

Abstract read
In one paragraph

Article in The Journal of general physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Musclin is an activity-stimulated myokine that enhances physical endurance.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  16. Article
  17. Article
  18. 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

14 authors.

Zhiyong ZhuDepartment of Internal Medicine and 2 Fraternal Order of Eagles Diabetes Research Center, University of Iowa Carver College of Medicine, Iowa City, IA 52242.
Ana Sierra
Colin M-L Burnett
Biyi Chen
Ekaterina Subbotina
Siva Rama Krishna Koganti
Zhan Gao
Yuejin Wu
Mark E Anderson
Long-Sheng Song
David J Goldhamer
William A Coetzee
Denice M Hodgson-Zingman
Leonid V Zingman

Funding

Mitochondrial Calmodulin Kinase II in Physiology and DiseaseR01HL070250 · NHLBI · VANDERBILT UNIVERSITY · PI ANDERSON, MARK E · 2002 to 2017
$5.2M
T-tubule remodeling and Ca2+-dependent arrhythmogenesis in cardiomyopathies.R01HL090905 · NHLBI · UNIVERSITY OF IOWA · PI SONG, LONG-SHENG · 2008 to 2017
$4.0M
Methionine sulfoxide reductase A and oxidized CaMKII in structural heart diseaseR01HL079031 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2006 to 2015
$3.3M
Potassium Channels as Macromolecular ComplexesR01HL085820 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COETZEE, WILLIAM A, NEUBERT, THOMAS A · 2008 to 2013
$3.2M
CaMKII in Sinus Node Physiology and DiseaseR01HL096652 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2009 to 2016
$3.0M
KATP Channel Trafficking and CardioprotectionR01HL126905 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COETZEE, WILLIAM A · 2015 to 2018
$2.7M
Satellite Cell Development and PotentialR01AR052777 · NIAMS · UNIVERSITY OF CONNECTICUT STORRS · PI GOLDHAMER, DAVID J · 2005 to 2010
$2.1M
Oxidized CaMKII in Atrial FibrillationR01HL113001 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2012 to 2016
$1.9M
Control of KATP channel expression by CaMKII: role in heart failure resistanceR01HL113089 · NHLBI · UNIVERSITY OF IOWA · PI HODGSON-ZINGMAN, DENICE · 2012 to 2016
$1.9M
Skeletal muscle KATP channels determine bodily energy balanceR01DK092412 · NIDDK · UNIVERSITY OF IOWA · PI ZINGMAN, LEONID · 2012 to 2016
$1.6M
KATP channel regulation of bodily energy expenditure and weight maintenanceK08HL093368 · NHLBI · UNIVERSITY OF IOWA · PI ZINGMAN, LEONID · 2008 to 2012
$637k
KATP channel expression and localization in the progression of heart failureK08HL092286 · NHLBI · UNIVERSITY OF IOWA · PI HODGSON-ZINGMAN, DENICE · 2008 to 2012
$636k
BLRD VA I01 BX000718NHLBI NIH HHS HL070250NHLBI NIH HHS HL079031NHLBI NIH HHS HL085820NHLBI NIH HHS HL090905NHLBI NIH HHS HL092286NHLBI NIH HHS HL093368NHLBI NIH HHS HL096652NHLBI NIH HHS HL113001NHLBI NIH HHS HL113089NHLBI NIH HHS K08 HL092286NHLBI NIH HHS K08 HL093368NHLBI NIH HHS R01 HL070250NHLBI NIH HHS R01 HL079031NHLBI NIH HHS R01 HL085820NHLBI NIH HHS R01 HL090905NHLBI NIH HHS R01 HL096652NHLBI NIH HHS R01 HL113001NHLBI NIH HHS R01 HL113089NHLBI NIH HHS R01 HL126905NIAMS NIH HHS AR052777NIAMS NIH HHS R01 AR052777NIDDK NIH HHS DK092412NIDDK NIH HHS R01 DK092412
6 · The paper itself

Abstract

ATP-sensitive potassium (KATP) channels have the unique ability to adjust membrane excitability and functions in accordance with the metabolic status of the cell. Skeletal muscles are primary sites of activity-related energy consumption and have KATP channels expressed in very high density. Previously, we demonstrated that transgenic mice with skeletal muscle-specific disruption of KATP channel function consume more energy than wild-type littermates. However, how KATP channel activation modulates skeletal muscle resting and action potentials under physiological conditions, particularly low-intensity workloads, and how this can be translated to muscle energy expenditure are yet to be determined. Here, we developed a technique that allows evaluation of skeletal muscle excitability in situ, with minimal disruption of the physiological environment. Isometric twitching of the tibialis anterior muscle at 1 Hz was used as a model of low-intensity physical activity in mice with normal and genetically disrupted KATP channel function. This workload was sufficient to induce KATP channel opening, resulting in membrane hyperpolarization as well as reduction in action potential overshoot and duration. Loss of KATP channel function resulted in increased calcium release and aggravated activity-induced heat production. Thus, this study identifies low-intensity workload as a trigger for opening skeletal muscle KATP channels and establishes that this coupling is important for regulation of myocyte function and thermogenesis. These mechanisms may provide a foundation for novel strategies to combat metabolic derangements when energy conservation or dissipation is required.

Indexed as

Isometric ContractionPhysical ExertionAction PotentialsAnimalsCalciumKATP ChannelsMaleMiceMice, Inbred C57BLMuscle, SkeletalMyographySarcolemmaCalciumKATP ChannelsuK-ATP-1 potassium channel

Identifiers

PMID24344248
PMCPMC3874572

What OpenQuestion holds

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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.