Evidence map›Paper›PMID 30569336›Full record

ArticleDigestive diseases and sciences2019

Villus Growth, Increased Intestinal Epithelial Sodium Selectivity, and Hyperaldosteronism Are Mechanisms of Adaptation in a Murine Model of Short Bowel Syndrome.

Peggy Berlin, Johannes Reiner, Jakob Wobar, Karen Bannert, Änne Glass, Michael Walter, Manuela Bastian, Holger Sven Willenberg, Brigitte Vollmar, Ernst Klar and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Digestive diseases and sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  6. Dysbiosis and reduced small intestinal function are required to induce intestinal insufficiency in mice.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
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  11. Loss of Slfn3 induces a sex-dependent repair vulnerability after 50% bowel resection.American journal of physiology. Gastrointestinal and liver physiology · 2021
    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

13 authors at 2 institutions in 1 country.

Peggy BerlinDivision of Gastroenterology, Department of Medicine II, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.ORCID 0000-0001-8354-6970
Johannes ReinerDivision of Gastroenterology, Department of Medicine II, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany. johannes.reiner@med.uni-rostock.de.
Jakob WobarDivision of Gastroenterology, Department of Medicine II, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.
Karen BannertDivision of Gastroenterology, Department of Medicine II, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.
Änne GlassInstitute for Biostatistics and Informatics in Medicine and Ageing Research, Rostock University Medical Center, Ernst-Heydemann-Str. 8, 18057, Rostock, Germany.
Michael WalterInstitute for Clinical Chemistry and Laboratory Medicine, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.
Manuela BastianInstitute for Clinical Chemistry and Laboratory Medicine, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.
Holger Sven WillenbergDivision of Endocrinology and Metabolism, Department of Medicine II, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.
Brigitte VollmarInstitute of Experimental Surgery, Rostock University Medical Center, Schillingallee 69a, 18057, Rostock, Germany.
Ernst KlarDepartment of General, Thoracic, Vascular and Transplantation Surgery, Rostock University Medical Center, Schillingallee 35, 18057, Rostock, Germany.
Ursula SeidlerDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Georg LamprechtDivision of Gastroenterology, Department of Medicine II, Rostock University Medical Center, Ernst-Heydemann-Str. 6, 18057, Rostock, Germany.
Maria WitteDepartment of General, Thoracic, Vascular and Transplantation Surgery, Rostock University Medical Center, Schillingallee 35, 18057, Rostock, Germany.
University of Rostock · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundShort bowel syndrome results from extensive small bowel resection and induces adaptation of the remaining intestine. Ileocecal resection (ICR) is the most frequent situation in humans. Villus hypertrophy is one hallmark of mucosal adaptation, but the functional mechanisms of mucosal adaptation are incompletely understood.

aimsThe aim of the study was to characterize a clinically relevant model of short bowel syndrome but not intestinal failure in mice and to identify outcome predictors and mechanisms of adaptation.

methodsMale C57BL6/J mice underwent 40% ICR and were followed for 7 or 14 days. Small bowel transection served as control. All mice underwent autopsy. Survival, body weight, wellness score, stool water content, plasma aldosterone concentrations, and paracellular permeability were recorded.

resultsUnlike controls, resected mice developed significant diarrhea with increased stool water. This was accompanied by sustained weight loss throughout follow-up. Villus length increased but did not correlate positively with adaptation. Plasma aldosterone concentrations correlated inversely with body weight at day 14. After ICR, intestinal epithelial (i.e., tight junctional) sodium permeability was increased.

conclusions40% ICR results in moderate to severe short bowel syndrome. Successful adaptation to the short bowel situation involves villus elongation but does not correlate with the degree of villus elongation alone. In addition, increased intestinal epithelial sodium permeability facilitates sodium-coupled solute transport. Hyperaldosteronism correlates with the severity of weight loss, indicates volume depletion, and counterregulates water loss.

Indexed as

Disease Models, AnimalAnimalsHyperaldosteronismIntestinal MucosaMaleMiceMice, Inbred C57BLOrgan Culture TechniquesRandom AllocationShort Bowel SyndromeSodiumSodiumClinical outcomeIleocecal resectionIntestinal adaptationIntestinal failureMiceShort bowel syndrome

Identifiers

PMID30569336
PMCPMC6548203
OpenAlexW2905914036

What OpenQuestion holds

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LicenceCC BY
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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.