Evidence map›Paper›PMID 12813156›Full record

ArticleThe Journal of physiology2003

AMPK activation increases uncoupling protein-3 expression and mitochondrial enzyme activities in rat muscle without fibre type transitions.

Charles T Putman, Monika Kiricsi, Jean Pearcey, Ian M MacLean, Jeremy A Bamford, Gordon K Murdoch, Walter T Dixon, Dirk Pette

Abstract read
In one paragraph

Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 100 citations in OpenAlex.

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  14. β-Adrenergic stimulation does not activate p38 MAP kinase or induce PGC-1α in skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2013
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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

8 authors at 2 institutions in 2 countries.

Charles T PutmanExercise Biochemistry Laboratory, Faculty of Physical Education, University of Alberta, E-417 Van Vliet Centre, Edmonton, Alberta, Canada T6G 2H9. tputman@ualberta.ca
Monika Kiricsi
Jean Pearcey
Ian M MacLean
Jeremy A Bamford
Gordon K Murdoch
Walter T Dixon
Dirk Pette
University of Alberta · CAUniversity of Konstanz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study examined the effect of chronic activation of 5'-AMP-activated protein kinase (AMPK) on the metabolic profile, including uncoupling protein-3 (UCP-3) and myosin heavy chain (MHC)-based fibre phenotype of rodent fast-twitch tibialis anterior muscle. Sprague-Dawley rats were given daily injections of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), a known activator of AMPK, or vehicle (control) for 28 days. After AICAR treatment, UCP-3 expression at the mRNA level was elevated 1.6 +/- 0.1-fold (P < 0.006) and corresponded to a 3.3 +/- 0.2-fold increase in UCP-3 protein content (P < 0.0001). In addition, the activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial volume density, were elevated 1.6-fold (P < 0.006), while the activity of lactate dehydrogenase (EC 1.1.1.27) was reduced to 80 % of control (P < 0.02). No differences were detected after AICAR treatment in the activities of the glycolytic reference enzymes glyceraldehydephosphate dehydrogenase (EC 1.2.1.12) or phosphofructokinase (EC 2.7.1.11), nor were MHC-based fibre-type transitions observed, using immunohistochemical or electrophoretic analytical methods. These changes could not be attributed to variations in inter-organ signalling by metabolic substrates or insulin. We conclude that an AMPK-dependent pathway of signal transduction does mimic some of the metabolic changes associated with chronic exercise training, but does not affect expression of the MHC-based structural phenotype. Thus, the metabolic and MHC-based fibre types do not appear to be regulated in a co-ordinated way, but may be independently modified by different signalling pathways.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsCarrier ProteinsEnzyme ActivationIon ChannelsMaleMitochondrial ProteinsMitochondria, MuscleMultienzyme ComplexesMuscle Fibers, Fast-TwitchMuscle Fibers, Slow-TwitchMuscle, SkeletalMyosin Heavy ChainsPhosphorylationProtein Serine-Threonine KinasesAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesCarrier ProteinsIon ChannelsMitochondrial ProteinsMultienzyme ComplexesMyosin Heavy ChainsProtein Serine-Threonine KinasesRibonucleotidesRNA, MessengerUcp3 protein, ratUncoupling Protein 3

Identifiers

PMID12813156
PMCPMC2343134
OpenAlexW2011099046

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.