Evidence map›Paper›PMID 32533922›Full record

ArticleDevelopmental cell2020

Adrenergic-Independent Signaling via CHRNA2 Regulates Beige Fat Activation.

Heejin Jun, Yingxu Ma, Yong Chen, Jianke Gong, Shanshan Liu, Jine Wang, Alexander J Knights, Xiaona Qiao, Margo P Emont, X Z Shawn Xu and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. Advances in Adipose Tissue Biology.Endocrine reviews · 2026
    Review
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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

12 authors at 4 institutions in 2 countries.

Heejin JunLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Yingxu MaLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Department of Cardiology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410013, China.
Yong ChenUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Jianke GongLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; International Research Center for Sensory Biology and Technology of MOST, Key Laboratory of Molecular Biophysics of MOE, and College of Life Sciences and Technology, and Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.
Shanshan LiuLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Jine WangLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Alexander J KnightsLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Xiaona QiaoLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Huashan Hospital, Fudan University, Shanghai 200040, China.
Margo P EmontLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
X Z Shawn XuLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Shingo KajimuraUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Jun WuLife Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, USA. Electronic address: wujunz@umich.edu.
University of Michigan · USUniversity of California, San Francisco · USCentral South University · CNFudan University · CN

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Molecular mechanisms of UCP1-independent pathways in metabolic healthR01DK097441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Shingo Kajimura · 2012 to 2026
$5.9M
The role of immune-adipocyte cholinergic signaling during metabolic adaptation and dysfunctionR01DK107583 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WU, JUN · 2016 to 2024
$3.4M
Neural and genetic mechanisms underlying behavior in C. elegans - Administrative Supplement for Equipment PurchasesR35GM126917 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI XU, SHAWN · 2018 to 2025
$3.3M
Molecular control of beige fat heterogeneityR01DK125281 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAJIMURA, SHINGO · 2020 to 2023
$1.9M
NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK097441NIDDK NIH HHS R01 DK107583NIGMS NIH HHS R35 GM126917
6 · The paper itself

Abstract

Maintaining energy homeostasis upon environmental challenges, such as cold or excess calorie intake, is essential to the fitness and survival of mammals. Drug discovery efforts targeting β-adrenergic signaling have not been fruitful after decades of intensive research. We recently identified a new beige fat regulatory pathway mediated via the nicotinic acetylcholine receptor subunit CHRNA2. Here, we generated fat-specific Chrna2 KO mice and observed thermogenic defects in cold and metabolic dysfunction upon dietary challenges caused by adipocyte-autonomous regulation in vivo. We found that CHRNA2 signaling is activated after acute high fat diet feeding and this effect is manifested through both UCP1- and creatine-mediated mechanisms. Furthermore, our data suggested that CHRNA2 signaling may activate glycolytic beige fat, a subpopulation of beige adipocytes mediated by GABPα emerging in the absence of β-adrenergic signaling. These findings reveal the biological significance of the CHRNA2 pathway in beige fat biogenesis and energy homeostasis.

Indexed as

Signal TransductionThermogenesisAdipocytes, BeigeAnimalsCell LineCells, CulturedCreatineGA-Binding Protein Transcription FactorHumansMiceMice, Inbred C57BLReceptors, Adrenergic, betaReceptors, NicotinicUncoupling Protein 1CHRNA2 protein, mouseCreatineGA-Binding Protein Transcription FactorGabpa protein, mouseReceptors, Adrenergic, betaReceptors, NicotinicUcp1 protein, mouseUncoupling Protein 1beige fatCHRNA2diet-induced thermogenesisg-beige fat

Identifiers

PMID32533922
PMCPMC7343629
OpenAlexW3035644891

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.