Evidence map›Paper›PMID 40459008›Full record

ArticleeLife2025

HNF4α-TET2-FBP1 axis contributes to gluconeogenesis and type 2 diabetes.

Hongchen Li, Xinchao Zhang, Xiaoben Liang, Shuyan Li, Ziyi Cui, Xinyu Zhao, Kai Wang, Bingbing Zha, Haijie Ma, Ming Xu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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.

Hongchen Li *Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0003-2639-8726
Xinchao Zhang *Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Xiaoben Liang *Tongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Shuyan LiDepartment of Radiation Oncology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Ziyi CuiTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Xinyu ZhaoTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Kai WangDepartment of Endocrinology, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Bingbing ZhaDepartment of Endocrinology, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Haijie MaCellular and Molecular Biology Laboratory, Affiliated Zhoushan Hospital of Wenzhou Medical University, Zhoushan, China.
Ming XuDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, United States.ORCID https://orcid.org/0000-0002-4477-939X
Lei LvMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-4820-3125
Yanping XuTongji Hospital, Frontier Science Center for Stem Cell Research, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0003-2750-5466

Funding

National Key Research and Development Program of China 2020YFA0803400/2020YFA0803402National Key Research and Development Program of China 2022YFA0807100National Natural Science Foundation of China 81972620National Natural Science Foundation of China 82073128National Natural Science Foundation of China 82121004National Natural Science Foundation of China 82172936National Natural Science Foundation of China 82372754National Natural Science Foundation of China 82472850Shanghai Rising-Star Program 24QA2709900
6 · The paper itself

Abstract

The control of gluconeogenesis is critical for glucose homeostasis and the pathology of type 2 diabetes (T2D). Here, we uncover a novel function of TET2 in the regulation of gluconeogenesis. In mice, both fasting and a high-fat diet (HFD) stimulate the expression of TET2, and

Indexed as

Diabetes Mellitus, Type 2DNA-Binding ProteinsGluconeogenesisHepatocyte Nuclear Factor 4Proto-Oncogene ProteinsAnimalsDiet, High-FatDioxygenasesHumansLiverMaleMetforminMiceMice, Inbred C57BLMice, KnockoutDioxygenasesDNA-Binding ProteinsHepatocyte Nuclear Factor 4Hnf4a protein, mouseMetforminProto-Oncogene ProteinsTet2 protein, mousecell biologydiabetesFBP1gluconeogenesisHNF4αmouseTET2

Identifiers

PMID40459008
PMCPMC12133150

What OpenQuestion holds

Texttitle and abstract
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 OpenQuestion graph.