Evidence map›Paper›PMID 41479596›Full record

ReviewDrug design, development and therapy2025

Xenin-Derived Peptides: Multifaceted Regulators and Therapeutic Innovations in Metabolic Diseases.

Binbin Gong, Xiyu Liu, Guoqiang Hu, Tongtong Li, Fei Chen, Xueqing Sun, Lidan Sun, Yinghe Xu

Abstract readReview
In one paragraph

Review in Drug design, development and therapy, 2025. 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.

Binbin Gong *Taizhou Hospital, Zhejiang University, Taizhou, 317000, People's Republic of China.
Xiyu Liu *Taizhou Hospital, Zhejiang University, Taizhou, 317000, People's Republic of China.ORCID 0009-0004-5658-1470
Guoqiang HuTaizhou Hospital, Zhejiang University, Taizhou, 317000, People's Republic of China.
Tongtong LiCollege of Medicine, Jiaxing University, Jiaxing, 314001, People's Republic of China.
Fei ChenCollege of Medicine, Jiaxing University, Jiaxing, 314001, People's Republic of China.
Xueqing SunCollege of Medicine, Jiaxing University, Jiaxing, 314001, People's Republic of China.
Lidan SunTaizhou Hospital, Zhejiang University, Taizhou, 317000, People's Republic of China.
Yinghe XuTaizhou Hospital, Zhejiang University, Taizhou, 317000, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Xenin, a 25-amino acid peptide hormone predominantly secreted by intestinal K cells, demonstrates evolutionary conservation with neuropeptides such as xenopsin and neurotensin. Functionally, it engages neurotensin receptor 1 (NTSR1) to regulate appetite via hypothalamic signaling pathways and modulates glucose homeostasis through synergistic interactions with incretin hormones. Preclinical studies highlight its dual role in suppressing appetite and enhancing pancreatic β-cell survival, while a single pilot human study suggests xenin-25 may delay gastric emptying and attenuate postprandial glucose excursions; however, these data await independent confirmation. Native xenin, however, is constrained by rapid proteolytic degradation and limited bioavailability. Advances in peptide engineering, including C-terminal truncation, site-directed amino acid substitution, and lipidation, have generated analogues that exhibit prolonged metabolic activity in rodent models, with plasma half-life extended from minutes to hours. In murine models of metabolic dysfunction, these derivatives enhance insulin secretion, improve glycaemic profiles and restore incretin responsiveness. Furthermore, multi-agonist peptides combining xenin with other gastrointestinal hormones show synergistic potential in preclinical studies, concurrently augmenting insulin secretion and reducing energy intake, though their clinical relevance remains to be validated in human trials. Despite promising preclinical outcomes, challenges persist in translating xenin-based therapies to clinical practice, including incomplete mechanistic insights into receptor cross-talk and species-specific variations in gastrointestinal responses. This review uniquely integrates the preclinical landscape of xenin biology, peptide-engineering principles, and emerging multi-agonist design, identifying knowledge gaps critical for future translation. We conclude that xenin-based therapeutics are a promising yet early-stage strategy whose efficacy and safety in human metabolic diseases remain to be established through rigorous pharmacokinetic profiling and phased clinical trials.

Indexed as

Metabolic DiseasesNeurotensinPeptidesAnimalsHumansNeurotensinPeptidesxenin 25obesityphysiological functionstructural modificationtype 2 diabetesXenin

Identifiers

PMID41479596
PMCPMC12755099

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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.