Evidence map›Paper›PMID 22798489›Full record

ArticleGenetics2012

Energy-dependent modulation of glucagon-like signaling in Drosophila via the AMP-activated protein kinase.

Jason T Braco, Emily L Gillespie, Gregory E Alberto, Jay E Brenman, Erik C Johnson

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

42 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Muscle PARP1 inhibition extends lifespan through AMPKα PARylation and activation inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Article
  5. Article
  6. Frontiers in medicine · 2022
    Review
  7. Article
  8. Insects as a New Complex Model in Hormonal Basis of Obesity.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. The Glucagon-Like Adipokinetic Hormone inFrontiers in physiology · 2021
    Review
  15. AKH Signaling inFrontiers in physiology · 2021
    Article
  16. Metabolism and growth adaptation to environmental conditions in Drosophila.Cellular and molecular life sciences : CMLS · 2020
    Review
  17. Review
  18. Regulation of insulin and adipokinetic hormone/glucagon production in flies.Wiley interdisciplinary reviews. Developmental biology · 2020
    Review
  19. 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

5 authors at 2 institutions in 2 countries.

Jason T BracoDepartment of Biology, Wake Forest University, Winston-Salem, NC 27109, USA.
Emily L Gillespie
Gregory E Alberto
Jay E Brenman
Erik C Johnson
Toxicologie, Pharmacologie et Signalisation Cellulaire · FRUniversity of North Carolina at Chapel Hill · US

Funding

Genetic Elucidation of AMP-Activated Protein Kinase Signaling MechanismsR01NS080108 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BRENMAN, JAY · 2012 to 2016
$1.6M
NINDS NIH HHS NS080108NINDS NIH HHS R01 NS080108
6 · The paper itself

Abstract

Adipokinetic hormone (AKH) is the equivalent of mammalian glucagon, as it is the primary insect hormone that causes energy mobilization. In Drosophila, current knowledge of the mechanisms regulating AKH signaling is limited. Here, we report that AMP-activated protein kinase (AMPK) is critical for normal AKH secretion during periods of metabolic challenges. Reduction of AMPK in AKH cells causes a suite of behavioral and physiological phenotypes resembling AKH cell ablations. Specifically, reduced AMPK function increases life span during starvation and delays starvation-induced hyperactivity. Neither AKH cell survival nor gene expression is significantly impacted by reduced AMPK function. AKH immunolabeling was significantly higher in animals with reduced AMPK function; this result is paralleled by genetic inhibition of synaptic release, suggesting that AMPK promotes AKH secretion. We observed reduced secretion in AKH cells bearing AMPK mutations employing a specific secretion reporter, confirming that AMPK functions in AKH secretion. Live-cell imaging of wild-type AKH neuroendocrine cells shows heightened excitability under reduced sugar levels, and this response was delayed and reduced in AMPK-deficient backgrounds. Furthermore, AMPK activation in AKH cells increases intracellular calcium levels in constant high sugar levels, suggesting that the underlying mechanism of AMPK action is modification of ionic currents. These results demonstrate that AMPK signaling is a critical feature that regulates AKH secretion, and, ultimately, metabolic homeostasis. The significance of these findings is that AMPK is important in the regulation of glucagon signaling, suggesting that the organization of metabolic networks is highly conserved and that AMPK plays a prominent role in these networks.

Indexed as

AMP-Activated Protein KinasesGlucagonInsect HormonesOligopeptidesAnimalsCell SurvivalDrosophila melanogasterGene Expression RegulationNeuroendocrine CellsPyrrolidonecarboxylic AcidSignal Transductionadipokinetic hormoneAMP-Activated Protein KinasesGlucagonInsect HormonesOligopeptidesPyrrolidonecarboxylic Acid

Identifiers

PMID22798489
PMCPMC3454876
OpenAlexW1974318258

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.