Evidence map›Paper›PMID 23263987›Full record

ArticleMolecular and cellular biology2013

Enhanced leptin sensitivity, reduced adiposity, and improved glucose homeostasis in mice lacking exchange protein directly activated by cyclic AMP isoform 1.

Jingbo Yan, Fang C Mei, Hongqiang Cheng, Dieu Hung Lao, Yaohua Hu, Jingna Wei, Igor Patrikeev, Dapeng Hao, Sonja J Stutz, Kelly T Dineley and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
1.9field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Review
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  12. Leptin signaling and leptin resistance.Medical review (2021) · 2022
    Review
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7 more citing papers are in PubMed but not listed here.

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

15 authors at 5 institutions in 3 countries.

Jingbo YanDepartment of Pharmacology and Toxicology, Sealy Center for Structural Biology and Molecular Biophysics, The University of Texas Medical Branch, Galveston, Texas, USA.
Fang C Mei
Hongqiang Cheng
Dieu Hung Lao
Yaohua Hu
Jingna Wei
Igor Patrikeev
Dapeng Hao
Sonja J Stutz
Kelly T Dineley
Massoud Motamedi
Jonathan D Hommel
Kathryn A Cunningham
Ju Chen
Xiaodong Cheng
The University of Texas Medical Branch at Galveston · USUniversity of California, San Diego · USClinical Research Services · DEQingdao University · CNZhejiang University · CN

Funding

Vinculin and Talin in Cardiocyte Integrity and AdhesionP01HL046345 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, JU · 1992 to 2011
$25.0M
Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
Epac/cAMP-GEF, A Novel Intracellular cAMP ReceptorR01GM066170 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CHENG, XIAODONG · 2003 to 2017
$4.6M
Addiction and the Neuropharmacology of PsychostimulantsK05DA020087 · NIDA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CUNNINGHAM, KATHRYN A. · 2005 to 2015
$1.3M
NHLBI NIH HHS P01 HL046345NHLBI NIH HHS P01 HL080101NHLBI NIH HHS P01 HL46345NIDA NIH HHS K05 DA020087NIDA NIH HHS K05DA020087NIGMS NIH HHS 5R01GM066170NIGMS NIH HHS R01 GM066170
6 · The paper itself

Abstract

The prototypic second messenger cyclic AMP (cAMP) is essential for controlling cellular metabolism, including glucose and lipid homeostasis. In mammals, the majority of cAMP functions are mediated by cAMP-dependent protein kinase (PKA) and exchange proteins directly activated by cAMP (Epacs). To explore the physiological functions of Epac1, we generated Epac1 knockout mice. Here we report that Epac1 null mutants have reduced white adipose tissue and reduced plasma leptin levels but display heightened leptin sensitivity. Epac1-deficient mice are more resistant to high-fat diet-induced obesity, hyperleptinemia, and glucose intolerance. Furthermore, pharmacological inhibition of Epac by use of an Epac-specific inhibitor reduces plasma leptin levels in vivo and enhances leptin signaling in organotypic hypothalamic slices. Taken together, our results demonstrate that Epac1 plays an important role in regulating adiposity and energy balance.

Indexed as

Adipose Tissue, WhiteAdiposityAnimalsCyclic AMPDiet, High-FatGene Knockout TechniquesGlucoseGlucose Tolerance TestGuanine Nucleotide Exchange FactorsLeptinMaleMiceMice, Inbred C57BLMice, KnockoutObesitySignal TransductionCyclic AMPEpac protein, mouseGlucoseGuanine Nucleotide Exchange FactorsLeptin

Identifiers

PMID23263987
PMCPMC3623083
OpenAlexW2130800855

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.