Evidence map›Paper›PMID 26824904›Full record

ArticlePloS one2016

AMP-Activated Protein Kinase Regulates Oxidative Metabolism in Caenorhabditis elegans through the NHR-49 and MDT-15 Transcriptional Regulators.

Elizabeth Moreno-Arriola, Mohammed El Hafidi, Daniel Ortega-Cuéllar, Karla Carvajal

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  5. Review
  6. Maackiain Mimics Caloric Restriction throughInternational journal of molecular sciences · 2023
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  8. Nutrients · 2023
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  11. PasteurizedMolecules (Basel, Switzerland) · 2022
    Article
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  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Mitochondrial retrograde signalling in neurological disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
  20. 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

4 authors at 2 institutions in 1 country.

Elizabeth Moreno-ArriolaLaboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Mexico City, Mexico.
Mohammed El HafidiDepartamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología, Mexico City, Mexico.
Daniel Ortega-CuéllarLaboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Mexico City, Mexico.
Karla CarvajalLaboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Mexico City, Mexico.
Instituto Nacional de Pediatria · MXInstituto Nacional de Cardiología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular energy regulation relies on complex signaling pathways that respond to fuel availability and metabolic demands. Dysregulation of these networks is implicated in the development of human metabolic diseases such as obesity and metabolic syndrome. In Caenorhabditis elegans the AMP-activated protein kinase, AAK, has been associated with longevity and stress resistance; nevertheless its precise role in energy metabolism remains elusive. In the present study, we find an evolutionary conserved role of AAK in oxidative metabolism. Similar to mammals, AAK is activated by AICAR and metformin and leads to increased glycolytic and oxidative metabolic fluxes evidenced by an increase in lactate levels and mitochondrial oxygen consumption and a decrease in total fatty acids and lipid storage, whereas augmented glucose availability has the opposite effects. We found that these changes were largely dependent on the catalytic subunit AAK-2, since the aak-2 null strain lost the observed metabolic actions. Further results demonstrate that the effects due to AAK activation are associated to SBP-1 and NHR-49 transcriptional factors and MDT-15 transcriptional co-activator, suggesting a regulatory pathway that controls oxidative metabolism. Our findings establish C. elegans as a tractable model system to dissect the relationship between distinct molecules that play a critical role in the regulation of energy metabolism in human metabolic diseases.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell RespirationEnergy MetabolismFatty AcidsGene Expression RegulationGlucoseHumansLactic AcidLongevityMetforminMitochondriaOxygenAAK-2 protein, C elegansAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesCaenorhabditis elegans ProteinsFatty AcidsGlucoseLactic AcidMDT-15 protein, C elegansMetforminNHR-49 protein, C elegansOxygenProtein Serine-Threonine KinasesProtein SubunitsReceptors, Cytoplasmic and NuclearRibonucleotidesSBP-1 protein, C elegansTranscription Factors

Identifiers

PMID26824904
PMCPMC4732773
OpenAlexW2408378333

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.