Evidence map›Paper›PMID 32485681›Full record

ReviewThe Journal of endocrinology2020

PKA functions in metabolism and resistance to obesity: lessons from mouse and human studies.

Edra London, Michelle Bloyd, Constantine A Stratakis

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Signaling architecture of the glucagon-like peptide-1 receptor.The Journal of clinical investigation · 2026
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  5. AnResearch square · 2026
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  6. Review
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  8. Anti-Obesity and Metabolic Effects of Forskolin in Obese C57BL/6J Mice.International journal of molecular sciences · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  13. Genetic Predisposition and Severity of Eating Disorders- A Review.CNS & neurological disorders drug targets · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

3 authors at 2 institutions in 1 country.

Edra LondonSection on Endocrinology and Genetics WEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.
Michelle BloydSection on Endocrinology and Genetics WEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.
Constantine A StratakisSection on Endocrinology and Genetics WEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Intramural NIH HHS Z99 DK999999
6 · The paper itself

Abstract

Both direct and indirect evidence demonstrate a central role for the cAMP-dependent protein kinase (PKA) signaling pathway in the regulation of energy balance and metabolism across multiple systems. However, the ubiquitous pattern of PKA expression across cell types poses a challenge in pinpointing its tissue-specific regulatory functions and further characterizing its many downstream effects in certain organs or cells. Mouse models of PKA deficiency and over-expression and studies in living cells have helped clarify PKA function in adipose tissue (AT), liver, adrenal, pancreas, and specific brain nuclei, as they pertain to energy balance and metabolic dysregulation. Limited studies in humans suggest differential regulation of PKA in AT of obese compared to lean individuals and an overall dysregulation of PKA signaling in obesity. Despite its complexity, under normal physiologic conditions, the PKA system is tightly regulated by changes in cAMP concentrations upstream via adenylate cyclase and downstream by phosphodiesterase-mediated cAMP degradation to AMP and by changes in PKA holoenzyme stability. Adjustments in the PKA system appear to be important to the development and maintenance of the obese state and its associated metabolic perturbations. In this review we discuss the important role of PKA in obesity and its involvement in resistance to obesity, through studies in humans and in mouse models, with a focus on the regulation of PKA in energy expenditure, intake behavior, and lipid and glucose metabolism.

Indexed as

Adipose TissueAnimalsCyclic AMP-Dependent Protein KinasesEnergy MetabolismHumansLipid MetabolismMiceObesityCyclic AMP-Dependent Protein Kinasesenergy balanceHPA axismetabolismobesityPKA

Identifiers

PMID32485681
PMCPMC7385994
OpenAlexW3026444766

What OpenQuestion holds

Textmetadata
LicenceTDM
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.