Evidence map›Paper›PMID 41343575›Full record

ArticlePLoS biology2025

The suprachiasmatic nucleus regulates brown fat thermogenesis in male mice through an adrenergic receptor ADRB3-S100B signaling pathway.

Yizhun Zeng, Xiaopeng Song, Qi Chen, Yue Gu, Jie Zhang, Tao Zhou, Zhihao Li, Tao Wang, Le Chang, Hongwei Yao and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

18 authors.

Yizhun ZengCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Xiaopeng SongCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Qi ChenCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Yue GuCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Jie ZhangCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Tao ZhouCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Zhihao LiCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Tao WangCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Le ChangCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Hongwei YaoInstitute of Molecular Enzymology, School of Life Sciences, Medical School of Soochow University, Suzhou, Jiangsu, China.
Yan WangDepartment of Clinical Pharmacology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Liyan MiaoDepartment of Clinical Pharmacology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Liujia QianSchool of Medicine, Westlake University, Hangzhou, Zhejiang Province, China.
Tiannan GuoSchool of Medicine, Westlake University, Hangzhou, Zhejiang Province, China.
Yong ZhangCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.
Sonia Rodriguez-FernandezUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.
Antonio Vidal-PuigUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.
Ying XuCambridge-Su Genomic Resource Center, The Fourth Affiliated Hospital of Soochow University, Medical School of Soochow University, Suzhou, Jiangsu, China.ORCID 0000-0002-6689-7768

Funding

Interdisciplinary Basic Frontier Innovation Program of Suzhou Medical College of Soochow UniversityLingang Laboratory & National Key Laboratory of Human Factors Engineering Joint GrantNational Key R&D program of ChinaNational Natural Science Foundation of China
6 · The paper itself

Abstract

The suprachiasmatic nucleus (SCN), the central circadian pacemaker, orchestrates daily metabolic rhythms, yet its role in substrate selection and thermogenic adaptation under stress remains insufficiently understood. Here, we show that SCN lesioning abolishes the adaptive suppression of brown adipose tissue (BAT) thermogenesis typically observed during time-restricted feeding in subthermoneutral environments (TRF-STE), a paradigm that imposes concurrent nutrient and thermal stress. Contrary to wild-type responses, SCN-lesioned mice maintain elevated BAT thermogenic activity, despite impaired lipolysis, instead shifting toward glucose-driven heat production. This phenotype is accompanied by sustained sympathetic tone and β3-adrenergic receptor (ADRB3) signaling in BAT. Mechanistically, we identify a SCN-regulated ADRB3-S100B signaling axis underlying this metabolic reprogramming. S100B, a nutrient-sensitive calcium-binding protein, is upregulated in BAT following SCN disruption, where it promotes thermogenesis by stimulating brown adipocyte proliferation and suppressing senescence. Functional studies reveal that S100B is both necessary and sufficient for sustaining BAT thermogenesis under TRF-STE. Furthermore, diverse SCN disruption models, including light-induced circadian arrhythmia, N-Methyl-D-aspartic acid (NMDA) excitotoxicity, and Caspase-3-mediated ablation, consistently elevate S100B expression in BAT, reinforcing its role as a convergent effector of SCN-regulated metabolic adaptation. Thus, in intact animal, the SCN restrains the ADRB3-S100B module, gating BAT thermogenic output in accordance with energetic availability. Disruption of SCN output lifts this restraint, unmasking a latent ADRB3-S100B program that preserves thermogenesis when lipid fuel is limited. These findings reveal a previously unrecognized role of the SCN in governing thermogenic flexibility and fuel partitioning, and position the ADRB3-S100B axis as a potential target for mitigating circadian misalignment and metabolic disease.

Indexed as

Adipose Tissue, BrownReceptors, Adrenergic, beta-3S100 Calcium Binding Protein beta SubunitSuprachiasmatic NucleusThermogenesisAnimalsCircadian RhythmMaleMiceMice, Inbred C57BLSignal TransductionAdrb3 protein, mouseReceptors, Adrenergic, beta-3S100b protein, mouseS100 Calcium Binding Protein beta Subunit

Identifiers

PMID41343575
PMCPMC12688110

What Socratic 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 Socratic graph.