Evidence map›Paper›PMID 42866259›Full record

ArticleiScience2026

Short term overfeeding disrupts small intestinal barrier integrity and activates hepatic immunity in healthy men.

Nora S Nägele, Malte P Suppli, Hannah Gilliam-Vigh, Natalia Petersen, Bolette Hartmann, Filip K Knop, Asger B Lund, Benjamin A H Jensen

Registry-linked trialAbstract 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. It is linked to trial NCT04859322 (The Effect of Lifestyle-induced Hepatic Steatosis on Glucagon-stimulated Amino Acid Turnover), which is not on this 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.

NCT04859322 nacompletednot on this map

The Effect of Lifestyle-induced Hepatic Steatosis on Glucagon-stimulated Amino Acid Turnover

TypeinterventionalSponsorMalte Palm Suppli, MDRan2021 to 2021Enrolled20ConditionsNon-Alcoholic Fatty Liver Disease, Glucagon ResistanceArmsGlucagon
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.

Nora S NägeleDepartment of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.
Malte P SuppliCenter for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, 2900 Hellerup, Denmark.
Hannah Gilliam-VighDepartment of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.
Natalia PetersenNovo Nordisk, 2760 Måløv, Denmark.
Bolette HartmannDepartment of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.
Filip K KnopCenter for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, 2900 Hellerup, Denmark.
Asger B LundCenter for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, 2900 Hellerup, Denmark.
Benjamin A H JensenDepartment of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is associated with intestinal barrier dysfunction and low-grade inflammation, prompting investigations of early human adaptations to overnutrition. In a controlled "holiday-style" overfeeding model, healthy men underwent a 2-week hypercaloric, sedentary lifestyle with 8-week follow-up (ClinicalTrials.gov NCT04859322). A targeted gastrointestinal uptake and translocation (GUT) plasma panel showed increased citrulline, consistent with enhanced epithelial absorptive capacity, and mucosa-restricted immune activation, reflected by elevated anti-lipopolysaccharide (LPS) immunoglobulin (Ig)A, without systemic 16S rRNA changes. A dynamic zonulin-like signal and hepatic inflammatory markers (serum amyloid A (SAA), C-reactive protein, interleukin-32) also increased after overfeeding. Most perturbations normalized after return to habitual lifestyle, but anti-LPS IgA, SAA, lipocalin-2, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 remained elevated, indicating a partially persistent inflammatory imprint. These findings reveal how overfeeding episodes reshape epithelial, mucosal, and hepatic immune responses and highlight plasma biomarker panels as scalable tools to interrogate intestinal function and gut-liver crosstalk in human studies.

Indexed as

barrier integrityhypercaloric dietintestinal inflammation

Identifiers

PMID42866259
PMCPMC13657223

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Registered trials

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.