Evidence map›Paper›PMID 25864946›Full record

ArticleNature communications2015

Regulation of systemic energy homeostasis by serotonin in adipose tissues.

Chang-Myung Oh, Jun Namkung, Younghoon Go, Ko Eun Shong, Kyuho Kim, Hyeongseok Kim, Bo-Yoon Park, Ho Won Lee, Yong Hyun Jeon, Junghan Song and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
11.9field-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

132 citing papers in PubMed, 254 citations in OpenAlex.

  1. Article
  2. Article
  3. New Updates in Adipocytes and Adipose Tissue.Life (Basel, Switzerland) · 2026
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72 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

17 authors at 8 institutions in 3 countries.

Chang-Myung OhBioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Jun NamkungBioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Younghoon GoDepartment of Internal Medicine, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-721, Korea.
Ko Eun ShongBioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Kyuho KimBioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Hyeongseok KimBioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Bo-Yoon ParkDepartment of Internal Medicine, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-721, Korea.
Ho Won LeeDepartment of Nuclear Medicine, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-721, Korea.
Yong Hyun JeonDepartment of Nuclear Medicine, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-721, Korea.
Junghan SongDepartment of Laboratory Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seoul 463-707, Korea.
Minho ShongResearch Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon 301-721, Korea.
Vijay K YadavWellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.
Gerard KarsentyDepartment of Genetics and Development, Columbia University Medical Center, New York, New York 10032, USA.
Shingo KajimuraDiabetes Center, Hormone Research Institute and Department of Medicine, University of California San Francisco, San Francisco, California 94143, USA.
In-Kyu LeeDepartment of Internal Medicine, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-721, Korea.
Sangkyu ParkBioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Hail KimBioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
Korea Advanced Institute of Science and Technology · KRKyungpook National University Hospital · KRCatholic Kwandong University · KRChungnam National University · KRColumbia University Irving Medical Center · USSeoul National University Bundang Hospital · KRUniversity of California, San Francisco · USWellcome Sanger Institute · GB

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 2003 to 2019
$21.8M
Molecular mechanisms of UCP1-independent pathways in metabolic healthR01DK097441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Shingo Kajimura · 2012 to 2026
$5.9M
NIDDK NIH HHS P30 DK063720NIDDK NIH HHS R01 DK097441
6 · The paper itself

Abstract

Central serotonin (5-HT) is an anorexigenic neurotransmitter in the brain. However, accumulating evidence suggests peripheral 5-HT may affect organismal energy homeostasis. Here we show 5-HT regulates white and brown adipose tissue function. Pharmacological inhibition of 5-HT synthesis leads to inhibition of lipogenesis in epididymal white adipose tissue (WAT), induction of browning in inguinal WAT and activation of adaptive thermogenesis in brown adipose tissue (BAT). Mice with inducible Tph1 KO in adipose tissues exhibit a similar phenotype as mice in which 5-HT synthesis is inhibited pharmacologically, suggesting 5-HT has localized effects on adipose tissues. In addition, Htr3a KO mice exhibit increased energy expenditure and reduced weight gain when fed a high-fat diet. Treatment with an Htr2a antagonist reduces lipid accumulation in 3T3-L1 adipocytes. These data suggest important roles for adipocyte-derived 5-HT in controlling energy homeostasis.

Indexed as

3T3-L1 CellsAdipocytes, BrownAdipocytes, WhiteAdipogenesisAdipose Tissue, BrownAdipose Tissue, WhiteAnimalsDiet, High-FatEnergy MetabolismEpididymisGene ExpressionHomeostasisMaleMiceMice, KnockoutObesityHtr3a protein, mouseReceptor, Serotonin, 5-HT2AReceptors, Serotonin, 5-HT3SerotoninTph1 protein, mouseTryptophan Hydroxylase

Identifiers

PMID25864946
PMCPMC4403443
OpenAlexW2050608961

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.