Evidence map›Paper›PMID 41340566›Full record

ArticleGut microbes2025

The microbial metabolite desaminotyrosine is a potent antiobesity agent with potential effects on white adipose tissue remodeling in mice.

Haohan Huang, Huimin Bu, Longxiang Liao, Yaoyao Xiang, Qiuchong Chen, Guiling Fu, Wanpeng Cheng, Yanbo Kou, Zhuanzhuan Liu, Kuiyang Zheng and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut microbes, 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

12 authors.

Haohan HuangJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Huimin BuJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Longxiang LiaoJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Yaoyao XiangJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Qiuchong ChenJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Guiling FuJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Wanpeng ChengJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Yanbo KouJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Zhuanzhuan LiuJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Kuiyang ZhengJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Yugang WangJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.
Yanxia WeiJiangsu Key Laboratory of Immunity and Metabolism, Jiangsu International Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesWhite adipose tissue plays a critical role in obesity, as its dysfunction can impair lipid homeostasis. We previously demonstrated that desaminotyrosine (DAT), a microbial metabolite, prevents high-fat diet (HFD)-induced body weight gain in mice, but the role of DAT on white adipocyte is unknown. Here, we investigated the role of DAT in host metabolic health and its therapeutic potentials in treating obesity.

methodsIn this study, we employed a pharmacological approach by administering DAT to mice. These mice were subjected to HFD feeding to establish overweight model, followed by DAT treatment. The effect of DAT on white adipocytes were studied using both in vivo and in vitro models.

resultsOur data indicated that DAT is a potent weight loss chemical for obesity treatment. This is related to DAT's dual-function in regulating white adipose tissue remodeling. DAT enhances mature white adipocyte-autonomous fat disposal through sustained lipolysis and augmented expression of carnitine palmitoyltransferase I family protein CPT1A, a critical enzyme facilitating fatty acid oxidation (FAO), especially under lipolytic-inducing conditions. In the meantime, it blocks white adipogenesis via FAO-dependent pathway potentiation.

conclusionsCollectively, these data demonstrate that DAT is a potent antiobesity agent with potential effects on white adipose tissue remodeling. This study provides a novel pharmacological strategy targeting white adipocyte plasticity for treating metabolic disorders.

Indexed as

Adipose Tissue, WhiteAnti-Obesity AgentsObesityTyrosineAdipocytes, WhiteAdipogenesisAnimalsDiet, High-FatDisease Models, AnimalLipid MetabolismLipolysisMaleMiceMice, Inbred C57BLAnti-Obesity AgentsTyrosineadipogenesisdesaminotyrosineenergy expenditurelipid metabolismobesityWhite adipocyte

Identifiers

PMID41340566
PMCPMC12688262

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.