Evidence map›Paper›PMID 40634590›Full record

ArticleCommunications medicine2025

Targeted in vivo gene integration of a secretion-enabled GLP-1 receptor agonist reverses diet-induced non-genetic obesity and pre-diabetes.

Jun Hirose, Emi Aizawa, Shogo Yamamoto, Shigenori Iwai, Keiichiro Suzuki

Abstract read
In one paragraph

Article in Communications medicine, 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
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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

5 authors.

Jun HiroseGraduate School of Engineering Science, The University of Osaka, Osaka, Japan.
Emi AizawaGraduate School of Engineering Science, The University of Osaka, Osaka, Japan.
Shogo YamamotoGraduate School of Engineering Science, The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0009-0001-8068-8620
Shigenori IwaiGraduate School of Engineering Science, The University of Osaka, Osaka, Japan.
Keiichiro SuzukiGraduate School of Engineering Science, The University of Osaka, Osaka, Japan. k.suzuki.es@osaka-u.ac.jp.ORCID http://orcid.org/0000-0001-5603-9105

Funding

Japan Agency for Medical Research and Development (AMED) JP23ek0109521MEXT | Japan Society for the Promotion of Science (JSPS) 21H04811; 22K19405
6 · The paper itself

Abstract

backgroundIn vivo genome editing offers a long-term therapeutic approach for monogenic diseases by directly modifying genetic sequences. However, its application to non-monogenic, noncommunicable diseases, which are the leading causes of global mortality, remains limited due to the lack of well-defined genetic targets.

methodsWe developed an in vivo genome-editing approach to introduce a gene encoding the glucagon-like peptide-1 (GLP-1) receptor agonist Exendin-4, modified with a secretion signal peptide. Mice with obesity and pre-diabetic conditions received a single administration of genome editing. Blood Exendin-4 levels, food intake, body weight, and metabolic parameters were monitored over several months.

resultsHere we show that in vivo genome editing enables sustained Exendin-4 secretion from liver cells, leading to prolonged elevation of Exendin-4 levels in the bloodstream. Treated mice exhibited reduced food intake, attenuated weight gain, and improved glucose metabolism and insulin sensitivity without detectable adverse effects.

conclusionsThis study demonstrates that a single administration of genome editing can achieve sustained therapeutic peptide secretion, providing a potential strategy for treating complex diseases without defined genetic causes.

Identifiers

PMID40634590
PMCPMC12241343

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.