Evidence map›Paper›PMID 41204980›Full record

ArticleDiabetologia2026

Peptide hormone spexin restores beta cell function and improves glycaemic control in mice via regulation of the sodium-potassium pump.

Yaojing Jiang, Di Wu, Yunzhi Ni, Ying Liu, Huixia Ren, Shan Liu, Chengfang Pan, Jiarong Dai, Quanya Sun, Anran Ma and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Emerging roles of spexin in cardiovascular homeostasis.Frontiers in cardiovascular medicine · 2026
    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

20 authors.

Yaojing Jiang *Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0004-9119-2745
Di Wu *Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-1802-4855
Yunzhi Ni *Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-2453-2522
Ying Liu *Department of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-9341-2674
Huixia RenCenter for Quantitative Biology and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China.ORCID http://orcid.org/0000-0002-1761-6018
Shan LiuDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0004-2999-6718
Chengfang PanSchool of Life Sciences, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0007-4503-8570
Jiarong DaiDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-2804-4019
Quanya SunDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-8446-4480
Anran MaInstitute of Endocrinology and Diabetes, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-1831-0851
Ge QinInstitute of Endocrinology and Diabetes, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0009-1876-0095
Jiali QianDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0001-3919-1225
Lijin JiDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0007-5264-179X
Hangping ZhengDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-2812-2176
Chao TangCenter for Quantitative Biology and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China.ORCID http://orcid.org/0000-0003-1474-3705
Yehong YangDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0003-3600-2174
Changlong HuSchool of Life Sciences, Fudan University, Shanghai, China. clhu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-8609-8947
Hao YinOrgan Transplant Center, Changzheng Hospital, Second Military Medical University, Shanghai, China. roytina0241032@hotmail.com.ORCID http://orcid.org/0009-0002-9286-7236
Yiming LiDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China. yimingli@fudan.edu.cn.ORCID http://orcid.org/0000-0002-1828-8765
Rui LiuDepartment of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China. fd_ruiliu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-8321-1617

Funding

Ministry of Science and Technology 2016YFC1305105National Natural Science Foundation of China 81200622National Natural Science Foundation of China 81800692National Natural Science Foundation of China 82070798National Science and Technology Major Project 2023ZD0506800Natural Science Foundation of Shanghai Municipality 21S11905200Natural Science Foundation of Shanghai Municipality 21SG35Natural Science Foundation of Shanghai Municipality SHDC12021116Natural Science Foundation of Shanghai Municipality SHDC2022CRD030
6 · The paper itself

Abstract

aims/hypothesisClinical studies revealed that serum spexin level is positively associated with beta cell function. However, the role of spexin in beta cells remains unclear. We hypothesise that spexin treatment could influence beta cell function and modulate glucose homeostasis in vivo.

methodsWe analysed glucose-stimulated insulin secretion (GSIS) and beta cell proliferation in mice and isolated mouse islets. Using mice fed a high-fat diet (HFD) and an HFD/streptozocin (STZ)-induced diabetes mouse model, we investigated the effects of spexin on glucose homeostasis and beta cell function. We performed a pull-down/MS assay and a cell-based binding assay to identify the binding partner of spexin on the beta cell surface. An ion pump activity assay and Atp1a1

resultsWe observed that spexin treatment increased GSIS in chow-diet-fed mice and isolated mouse islets. Spexin treatment also promoted beta cell proliferation in mouse islets and pancreatectomised mice. Furthermore, spexin treatment improved glucose tolerance in HFD-fed mice and attenuated hyperglycaemia in an HFD/STZ-induced diabetes mouse model, along with an elevated serum insulin level and increased beta cell proliferation. Spexin showed specific binding to the beta cell surface. The pull-down/MS assay demonstrated that spexin bound to the α1 subunit of sodium-potassium ATPase (ATP1A1), resulting in pump activity inhibition and subsequent membrane depolarisation. In Atp1a1 CONCLUSIONS/

interpretationOur study highlights that spexin is a stimulatory factor for beta cell function and proliferation, and suggests that spexin is a diabetes therapeutic target for beta cell intervention.

Indexed as

Insulin-Secreting CellsPeptide HormonesSodium-Potassium-Exchanging ATPaseAnimalsBlood GlucoseCell ProliferationDiabetes Mellitus, ExperimentalDiet, High-FatGlycemic ControlHumansInsulinInsulin SecretionMaleMiceMice, Inbred C57BLBlood GlucoseInsulinPeptide HormonesSodium-Potassium-Exchanging ATPaseDiabetesInsulin secretionProliferationSodium–potassium pumpSpexin

Identifiers

PMID41204980
PMCPMC12881104

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.