Evidence map›Paper›PMID 24914943›Full record

ArticleEndocrinology2014

Differentially regulated protein kinase A (PKA) activity in adipose tissue and liver is associated with resistance to diet-induced obesity and glucose intolerance in mice that lack PKA regulatory subunit type IIα.

Edra London, Maria Nesterova, Ninet Sinaii, Eva Szarek, Tatyana Chanturiya, Spyridon A Mastroyannis, Oksana Gavrilova, Constantine A Stratakis

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Mechanisms of Abnormal Lipid Metabolism in the Pathogenesis of Disease.International journal of molecular sciences · 2024
    Review
  2. Article
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  6. American journal of physiology. Endocrinology and metabolism · 2021
    Article
  7. Review
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  12. Review
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  16. The Catalytic SubunitJournal of the Endocrine Society · 2019
    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

8 authors at 3 institutions in 1 country.

Edra LondonSection on Endocrinology and Genetics (E.L., M.N., E.S., S.A.M., C.A.S.), Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Biostatistics and Clinical Epidemiology Service (N.S.), CC, National Institutes of Health, Mouse Metabolism Core Laboratory (T.C., O.G.), National Institute of Diabetes and Digestive and Kidney Diseases, and Eunice Kennedy Shriver National Institute of Child Health and Human Development intramural Summer Student Program (S.A.M.), Bethesda, Maryland 20892.
Maria Nesterova
Ninet Sinaii
Eva Szarek
Tatyana Chanturiya
Spyridon A Mastroyannis
Oksana Gavrilova
Constantine A Stratakis
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Molecular Genetics of Endocrine Tumors and Related DisordersZIAHD008920 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STRATAKIS, CONSTANTINE A. · 2012 to 2021
$25.8M
Metabolic Studies of Mouse Models of Obesity and DiabetesZICDK070002 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GAVRILOVA, OKSANA · 2009 to 2025
$15.0M
Intramural NIH HHS
6 · The paper itself

Abstract

The cAMP-dependent protein kinase A (PKA) signaling system is widely expressed and has a central role in regulating cellular metabolism in all organ systems affected by obesity. PKA has four regulatory (RIα, RIIα, RIβ, RIIβ) and four catalytic (Cα, Cβ, Cγ, Prkx) subunit isoforms that have tissue-specific expression profiles. In mice, knockout (KO) of RIIβ, the primary PKA regulatory subunit in adipose tissue or knockout of the catalytic subunit Cβ resulted in a lean phenotype that resists diet-induced obesity and associated metabolic complications. Here we report that the disruption of the ubiquitously expressed PKA RIIα subunit in mice (RIIαKO) confers resistance to diet-induced obesity, glucose intolerance, and hepatic steatosis. After 2-week high-fat diet exposure, RIIαKO mice weighed less than wild-type littermates. Over time this effect was more pronounced in female mice that were also leaner than their wild-type counterparts, regardless of the diet. Decreased intake of a high-fat diet contributed to the attenuated weight gain in RIIαKO mice. Additionally, RIIα deficiency caused differential regulation of PKA in key metabolic organs: cAMP-stimulated PKA activity was decreased in liver and increased in gonadal adipose tissue. We conclude that RIIα represents a potential target for therapeutic interventions in obesity, glucose intolerance, and nonalcoholic fatty liver disease.

Indexed as

Adipose TissueAnimalsCyclic AMP-Dependent Protein Kinase RIIalpha SubunitCyclic AMP-Dependent Protein KinasesDiet, High-FatFatty LiverFemaleGlucose IntoleranceHumansLiverMaleMiceMice, Inbred C57BLMice, KnockoutNon-alcoholic Fatty Liver DiseaseObesityCyclic AMP-Dependent Protein Kinase RIIalpha SubunitCyclic AMP-Dependent Protein Kinases

Identifiers

PMID24914943
PMCPMC4138573
OpenAlexW2017462401

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.