Evidence map›Paper›PMID 39905656›Full record

ArticleDiabetes & metabolism journal2025

Serotonin Regulates Lipogenesis and Endoplasmic Reticulum Stress in Alcoholic Liver Disease.

Inseon Hwang, Jung Eun Nam, Wonsuk Choi, Won Gun Choi, Eunji Lee, Hyeongseok Kim, Young-Ah Moon, Jun Yong Park, Hail Kim

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PubMed Full text at PMC Publisher
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Article in Diabetes & metabolism journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

9 authors.

Inseon Hwang *Department of Biopharmacy, Daejeon Health University, Daejeon, Korea.
Jung Eun Nam *Graduate School of Medical Science and Engineering, Biomedical Research Center, Korea Advanced Institute of Science and Technology, Daejeon, Korea.
Wonsuk ChoiDepartment of Internal Medicine, Chonnam National University Hwasun Hospital, Chonnam National University Medical School, Hwasun, Korea.
Won Gun ChoiDivision of Endocrinology and Metabolism, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Eunji LeeDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Hyeongseok KimDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Young-Ah MoonDepartment of Molecular Medicine, Inha University College of Medicine, Incheon, Korea.
Jun Yong ParkDepartment of Internal Medicine, Yonsei Liver Center, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Hail KimGraduate School of Medical Science and Engineering, Biomedical Research Center, Korea Advanced Institute of Science and Technology, Daejeon, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgruoundSerotonin (5-hydroxytryptamine [5-HT]) is a monoamine neurotransmitter that has various functions in central and peripheral tissues. While 5-HT is known to regulate various biological processes in liver, direct role of 5-HT and its receptors, especially 5-HT receptor 2A (HTR2A) and HTR2B, in development and progression of alcoholic liver disease (ALD) in vivo is not well understood.

methodsBlood 5-HT level was measured from both human ALD patients and ethanol (EtOH) diet-fed mouse models. Gut-specific tryptophan hydroxylase 1 (Tph1) knockout mice, liver-specific Htr2a knockout mice, and liver-specific Htr2b knockout mice were fed with EtOH diet. Then we evaluated liver damage, hepatic steatosis, endoplasmic reticulum (ER) stress, and inflammation.

resultsBlood 5-HT concentrations are increased in both humans and mice with ALD. Both gut-specific Tph1 knockout and liver- specific Htr2a knockout mice are resistant to steatosis by down-regulating lipogenic pathways in liver of chronic EtOH diet-fed mice. Moreover, genetic inhibition of both gut-derived serotonin (GDS) synthesis and hepatic HTR2A signaling prevents ER stress in liver of chronic EtOH diet-fed mice. Additionally, we found that ablation of HTR2A signaling protects against disease progression by attenuating liver injury and inflammation in chronic plus binge EtOH diet-fed mice. Also, inhibiting HTR2A signaling ameliorates alcohol-induced liver injury and ER stress in an acute EtOH diet-fed mice model.

conclusionGDS directly regulates lipogenesis and ER stress via signaling through hepatic HTR2A in the context of ALD. Inhibiting HTR2A signaling protects against alcohol-induced steatosis, liver injury and disease progression in various ALD mouse models and may also provide a novel therapeutic strategy for ALD.

Indexed as

Endoplasmic Reticulum StressLipogenesisLiver Diseases, AlcoholicSerotoninAnimalsDisease Models, AnimalFemaleHumansLiverMaleMiceMice, Inbred C57BLMice, KnockoutReceptor, Serotonin, 5-HT2AReceptor, Serotonin, 5-HT2BTryptophan HydroxylaseReceptor, Serotonin, 5-HT2AReceptor, Serotonin, 5-HT2BSerotoninTph1 protein, mouseTryptophan HydroxylaseAlcoholicsEndoplasmic reticulum stressFatty liverLiver diseasesReceptors, serotoninSerotoninTryptophan hydroxylase

Identifiers

PMID39905656
PMCPMC12270569

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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.