Evidence map›Paper›PMID 42803877›Full record

ArticleJournal of physiology and biochemistry2026

Cold-induced serum amyloid A3 amplifies cAMP-PKA signaling to drive adaptive thermogenesis in brown adipocytes.

Pei-Chi Chan, Hung-Che Chien, Pei-Ru Lin, Yu-Feng Tian, Po-Shiuan Hsieh

Abstract read
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Article in Journal of physiology and biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Pei-Chi ChanGraduate Institute of Medical Sciences, College of Medicine, National Defense Medical University (NDMU), 161, Section 6 Min-Chuan East Road, Taipei, 114, Taiwan.
Hung-Che ChienGraduate Institute of Physiology, College of Biomedical Sciences, NDMU, Taipei, 114, Taiwan.
Pei-Ru LinGraduate Institute of Physiology, College of Biomedical Sciences, NDMU, Taipei, 114, Taiwan.
Yu-Feng TianDivision of General Surgery, Department of Surgery, Chi-Mei Medical Center, Yung Kung Campus, Tainan, 710, Taiwan.
Po-Shiuan HsiehGraduate Institute of Medical Sciences, College of Medicine, National Defense Medical University (NDMU), 161, Section 6 Min-Chuan East Road, Taipei, 114, Taiwan. pshsieh@mail.ndmutsgh.edu.tw.

Funding

Cheng Hsin General Hospital Foundation CHNDMU-115-07Chi Mei Medical Center CMNDMC 108-03National Science and Technology Council 111-2320-B-016-003-MY3; 111-2320-B-016-016; 114-2320-B-016-005Tri-Service General Hospital TSGH-C04-113041; TSGH-C02-114032; TSGH-C02-115032
6 · The paper itself

Abstract

Serum amyloid A3 (SAA3) is typically associated with inflammation, but its role in brown adipose tissue (BAT) thermogenesis remains elusive. Here, we identify SAA3 as a cold-inducible, locally acting amplifier of BAT thermogenesis. Using lentiviral modulation and BAT-specific knockout mice, we demonstrate that SAA3 is essential for cold tolerance and energy expenditure. Mechanistically, secreted SAA3 augments thermogenic signaling via a GPR3-dependent cAMP/PKA axis, driving robust UCP1 induction. Notably, this activation triggers transcriptional upregulation of endogenous Saa3 and Gpr3, establishing an autocrine/paracrine amplification loop that accelerates thermogenic output. Consequently, SAA3 loss blunts thermogenic responses in vivo and in vitro. These findings establish SAA3 as a BAT-derived regulator linking cold exposure to energy dissipation via a GPR3-mediated mechanism, highlighting its therapeutic potential for metabolic diseases.

Indexed as

Adipocytes, BrownCold TemperatureCyclic AMPCyclic AMP-Dependent Protein KinasesSerum Amyloid A ProteinThermogenesisAdipose Tissue, BrownAnimalsEnergy MetabolismHumansMaleMiceMice, KnockoutReceptors, G-Protein-CoupledSignal TransductionUncoupling Protein 1Cyclic AMPCyclic AMP-Dependent Protein KinasesReceptors, G-Protein-CoupledSaa3 protein, mouseSerum Amyloid A ProteinUcp1 protein, mouseUncoupling Protein 1Acute phase proteinBrown adipose tissueCold-induced adaptive thermogenesisSerum Amyloid A-3

Identifiers

PMID42803877
PMCPMC13619661

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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.