Evidence map›Paper›PMID 41223989›Full record

ArticleJournal of advanced research2026

Loss of Slc39a5 in α-cells impairs glucose metabolism by chronically increasing glucagon.

Wenli Chen, Weiyi Cui, Yan Xu, Xuelian Wang, Xueting Sun, Jing Ren, Ning Hou, Wenyong Xiong, Rui-Ping Xiao, Xiuqin Zhang

Abstract read
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Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Wenli ChenInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China; Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education, Yunnan Key Laboratory of Research and Development for Natural Products, School of Pharmacy, Yunnan University, Kunming 650500, China.
Weiyi CuiInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China.
Yan XuInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China.
Xuelian WangInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China.
Xueting SunInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China.
Jing RenInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China.
Ning HouInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China.
Wenyong XiongKey Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education, Yunnan Key Laboratory of Research and Development for Natural Products, School of Pharmacy, Yunnan University, Kunming 650500, China. Electronic address: xwy@ynu.edu.cn.
Rui-Ping XiaoInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China; State Key Laboratory of Biomembrane and Membrane Biotechnology, Peking-Tsinghua Center for Life Sciences, Beijing 100871, China. Electronic address: xiaor@pku.edu.cn.
Xiuqin ZhangInstitute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China; Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking University, Beijing 100871, China; National Biomedical Imaging Center, School of Future Technology, Peking University, Beijing 100871, China. Electronic address: zhangxq@pku.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGlucagon is a critical regulator of glucose homeostasis by regulating liver glycogenolysis and gluconeogenesis. Hyperglucagonemia has been observed in patients with type 2 diabetes mellitus (T2DM). However, whether elevated glucagon is cause or consequence in the pathogenesis of T2DM is poorly investigated.

objectivesThis study aimed to investigate the metabolic effects of chronic glucagon elevation using a α-cells-specific Slc39a5 knockout mouse model.

methodsα-cells-specific Slc39a5 knockout mice (Slc39a5

resultsCompared with Slc39a5

conclusionsThese results demonstrate that Slc39a5 deficiency in α-cells leads to chronic glucagon elevation, which directly impairs hepatic glucose metabolism and promotes insulin resistance and hyperglycemia. This study thus establishes a causal role for α-cells Slc39a5 in prediabetes progression, highlighting sustained glucagon excess as a key contributor of metabolic dysfunction.

Indexed as

Cation Transport ProteinsDiabetes Mellitus, Type 2GlucagonGlucagon-Secreting CellsGlucoseAnimalsBlood GlucoseInsulin ResistanceLiverMaleMiceMice, KnockoutBlood GlucoseCation Transport ProteinsGlucagonGlucoseGlucagon secretionGlucose metabolismGlycogenesisInsulin resistanceSlc39a5

Identifiers

PMID41223989
PMCPMC13453833

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Registered trials

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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.