Evidence map›Paper›PMID 42894858›Full record

ArticleiScience2026

L-Histidine alleviates tacrolimus-induced islet dysfunction via the gut-pancreas axis.

Zhen Geng, Qiang Li, Duo Wang, Hongji Yang, Hailian Wang, Jinku Bao, Yi Wang, Liang Wei

Abstract read
In one paragraph

Article in iScience, 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
–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

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

8 authors.

Zhen GengKey Laboratory of BioResource and Eco-Environment of Ministry of Education, College of Life Science, Sichuan University, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Qiang LiDepartment of Gastrointestinal Surgery I Section, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Duo WangTranslational Clinical Immunology Medicine Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Hongji YangTranslational Clinical Immunology Medicine Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Hailian WangTranslational Clinical Immunology Medicine Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Jinku BaoKey Laboratory of BioResource and Eco-Environment of Ministry of Education, College of Life Science, Sichuan University, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Yi WangTranslational Clinical Immunology Medicine Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Liang WeiTransplantation Health Management Center, Sichuan Taikang Hospital, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tacrolimus is widely used after organ transplantation but can impair pancreatic β-cell function and glucose homeostasis. Using rodent models, antibiotic-mediated microbiota depletion, fecal microbiota transplantation, 16S rRNA sequencing, metabolomic profiling, and MIN-6 cells, we examined whether microbiota-associated L-histidine contributes to β-cell protection. Tacrolimus altered gut microbial composition and increased histidine-associated microbial and metabolic signals. L-histidine supplementation improved glucose tolerance and insulin secretion, reduced β-cell apoptosis, and increased PI3K/Akt/mTOR/p70S6K signaling and PDX-1, NeuroD1, and MafA expression. Microbiota depletion attenuated several protective effects of L-histidine, supporting a contribution of the gut microbiota to this response. These findings connect a microbiota-associated amino acid with tacrolimus-related β-cell dysfunction and provide a framework for investigating microbiota-metabolite contributions to metabolic complications of immunosuppression.

Indexed as

gut microbiotaL-histidinePDX-1/ NeuroD1/MafAPI3K/AKT/mTOR signaling pathwaytacrolimus-induced diabetes

Identifiers

PMID42894858
PMCPMC13677189

What OpenQuestion holds

Textmetadata
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.