Evidence map›Paper›PMID 29715464›Full record

ArticleMetabolism: clinical and experimental2018

Spermidine/spermine N1-acetyltransferase-mediated polyamine catabolism regulates beige adipocyte biogenesis.

Fang Yuan, Lin Zhang, Yang Cao, Wei Gao, Can Zhao, Yuan Fang, Kamyar Zahedi, Manoocher Soleimani, Xiang Lu, Zhuyuan Fang and 1 more

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

Article in Metabolism: clinical and experimental, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. SAT1-Induced Spermidine Depletion Potentiates Food Allergy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  13. The ESCRT-III ProteinMedical sciences (Basel, Switzerland) · 2022
    Article
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  17. A new signal that shrinks fat.Nature metabolism · 2022
    Article
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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

11 authors at 5 institutions in 2 countries.

Fang YuanFirst Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China; Department of Medicine, Physiology and Biophysics, Diabetes Center, Center for Epigenetics and Metabolism, University of California Irvine, Irvine, CA 92697, USA.
Lin ZhangDepartment of Medicine, Physiology and Biophysics, Diabetes Center, Center for Epigenetics and Metabolism, University of California Irvine, Irvine, CA 92697, USA; College of Animal Science, South China Agricultural University, Guangzhou 512642, China.
Yang CaoDepartment of Medicine, Physiology and Biophysics, Diabetes Center, Center for Epigenetics and Metabolism, University of California Irvine, Irvine, CA 92697, USA.
Wei GaoDepartment of Medicine, Physiology and Biophysics, Diabetes Center, Center for Epigenetics and Metabolism, University of California Irvine, Irvine, CA 92697, USA; Department of Geriatrics, Sir Run Run Shaw Hospital, Nanjing Medical University, Nanjing 211166, China.
Can ZhaoDepartment of Medicine, Physiology and Biophysics, Diabetes Center, Center for Epigenetics and Metabolism, University of California Irvine, Irvine, CA 92697, USA; Department of Geriatrics, Sir Run Run Shaw Hospital, Nanjing Medical University, Nanjing 211166, China.
Yuan FangFirst Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China; Department of Medicine, Physiology and Biophysics, Diabetes Center, Center for Epigenetics and Metabolism, University of California Irvine, Irvine, CA 92697, USA.
Kamyar ZahediDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Cincinnati College of Medicine, USA.
Manoocher SoleimaniDivision of Nephrology and Hypertension, Department of Internal Medicine, University of Cincinnati College of Medicine, USA.
Xiang LuDepartment of Geriatrics, Sir Run Run Shaw Hospital, Nanjing Medical University, Nanjing 211166, China.
Zhuyuan FangFirst Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China. Electronic address: jsszyyfzy@163.com.
Qin YangDepartment of Medicine, Physiology and Biophysics, Diabetes Center, Center for Epigenetics and Metabolism, University of California Irvine, Irvine, CA 92697, USA. Electronic address: qin.yang@uci.edu.
University of California, Irvine · USNanjing University of Chinese Medicine · CNUniversity of Cincinnati Medical Center · USNanjing Medical University · CNSir Run Run Shaw Hospital · CN

Funding

Nicotinamide N-methyltransferase is a novel regulator of energy expenditureR01DK100385 · NIDDK · UNIVERSITY OF CALIFORNIA-IRVINE · PI YANG, QIN · 2014 to 2018
$1.7M
NIDDK NIH HHS R01 DK100385
6 · The paper itself

Abstract

objectiveCold and β3-adrenergic receptor (AR) agonists activate beige adipocyte biogenesis in white adipose tissue (WAT). The two stimuli also induce expression of inflammatory cytokines in WAT. The low-grade inflammation may further promote WAT browning. However, the mechanisms to reconcile these two biological processes remain to be elucidated. In this study, we aim to investigate the roles of the rate-limiting polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase (SAT1) in regulating beige adipocyte biogenesis and inflammation.

methodsAdipose-specific SAT1 knockout mice (SAT1-aKO) were generated by crossing adiponectin-cre to SAT1-lox/lox mice. Metabolic phenotype was investigated. Primary pre-adipocytes were isolated from inguinal WAT (iWAT) and differentiated to adipocytes for studying beige adipocyte biogenesis.

resultThe expression and enzymatic activity of SAT1 were up-regulated in iWAT upon cold and β3-AR stimulation. SAT1-aKO mice developed late-onset obesity on a high-fat diet with impaired cold-induced beige adipocyte biogenesis and energy expenditure. RNA-seq analysis of iWAT from cold-challenged SAT1-aKO mice revealed that, in addition to beige adipocyte biogenesis signatures, the immune response markers were highly enriched among reduced genes. In cultured adipocytes, SAT1 overexpression or pharmacological activation with N1, N11-diethylnorspermine (DENSpm) elevated oxygen consumption and increased the expression of beige adipocyte marker UCP1 and PGC-1α. DENSpm treatment of adipocytes also increased the expression of inflammatory genes. SAT1 activation enhanced hydrogen peroxide production in adipocytes. Antioxidant N-acetylcysteine abrogated the elevated UCP1 expression and reversed some inflammatory genes induced by SAT1 activation.

conclusionsSAT1 activation plays a key role in cold and β3-AR agonist-induced beige adipocyte biogenesis and low-grade inflammation.

Indexed as

AcetyltransferasesAdipocytes, BeigeAnimalsDiamine N-AcetyltransferaseEnergy MetabolismHydrogen PeroxideInflammationLipid MetabolismMiceMice, KnockoutOxygen ConsumptionReactive Oxygen SpeciesThermogenesisUncoupling Protein 1AcetyltransferasesDiamine N-AcetyltransferaseHydrogen PeroxideReactive Oxygen SpeciesUncoupling Protein 1Beige adipocytesEnergy expenditureInflammationObesityPolyamine metabolism

Identifiers

PMID29715464
PMCPMC7269456
OpenAlexW2801685366

What OpenQuestion holds

Textmetadata
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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.