Evidence map›Paper›PMID 28946616›Full record

ArticleInternational journal of molecular sciences2017

Characterization of Growth Hormone Resistance in Experimental and Ulcerative Colitis.

Christoffer Soendergaard, Peter Helding Kvist, Peter Thygesen, Mats Reslow, Ole Haagen Nielsen, John Joseph Kopchick, Thomas Lindebo Holm

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  6. American journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. IGF-1 and IGFBP-3 in Inflammatory Cachexia.International journal of molecular sciences · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. COX-2-PGEEBioMedicine · 2018
    Article
  19. Review
  20. Article
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

7 authors at 3 institutions in 2 countries.

Christoffer SoendergaardNovo Nordisk A/S, Haemophilia Research, Maaloev 2760, Denmark. c.sondergaard@gmail.com.ORCID 0000-0002-2943-6911
Peter Helding KvistNovo Nordisk A/S, Haemophilia Research, Maaloev 2760, Denmark. PHKV@novonordisk.com.
Peter ThygesenNovo Nordisk A/S, Haemophilia Research, Maaloev 2760, Denmark. PTT@novonordisk.com.
Mats ReslowNovo Nordisk A/S, Haemophilia Research, Maaloev 2760, Denmark. MRSL@pilapharma.com.
Ole Haagen NielsenDepartment of Gastroenterology, Herlev Hospital, Herlev 2730, Denmark. Ole.Haagen.Nielsen@regionh.dk.
John Joseph KopchickEdison Biotechnology Institute & Department of Biomedical Sciences, HCOM, Ohio University, Athens, OH 45701, USA. kopchick@ohio.edu.
Thomas Lindebo HolmNovo Nordisk A/S, Haemophilia Research, Maaloev 2760, Denmark. thlh@novonordisk.com.
Novo Nordisk (Denmark) · DKBiotechnology Institute · USHerlev Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth hormone (GH) resistance may develop as a consequence of inflammation during conditions such as inflammatory bowel disease, encompassing ulcerative colitis (UC). However, the specific role of the GH-insulin growth factor (IGF)-1-axis and/or the functional consequences of GH resistance in this condition are unclear. In situ hybridization targeting the GH receptor (GHR) and relevant transcriptional analyses were performed in patients with UC and in IL-10 knock-out mice with piroxicam accelerated colitis (PAC). Using cultured primary epithelial cells, the effects of inflammation on the molecular mechanisms governing GH resistance was verified. Also, the therapeutic potential of GH on mucosal healing was tested in the PAC model. Inflammation induced intestinal GH resistance in UC and experimental colitis by down-regulating GHR expression and up-regulating suppressor of cytokine signalling (SOCS) proteins. These effects are driven by pro-inflammatory mediators (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6) as confirmed using primary epithelial cells. Treatment of experimental colitis with GH increased IGF-1 and body weight of the mice, but had no effects on colonic inflammation or mucosal healing. The high transcriptional similarity between UC and experimental colitis accentuates the formation of intestinal GH resistance during inflammation. Inflammation-induced GH resistance not only impairs general growth but induces a state of local resistance, which potentially impairs the actions of GH on mucosal healing during colitis when using long-acting GH therapy.

Indexed as

AdultAnimalsBiopsyCase-Control StudiesColitis, UlcerativeColonoscopyCytokinesDisease Models, AnimalFemaleGene ExpressionGrowth HormoneHumansImmunohistochemistryInflammation MediatorsInflammatory Bowel DiseasesIntestinal MucosaCytokinesGrowth HormoneInflammation MediatorsReceptors, Somatotropinexperimental colitisGHRGH resistanceIGF-1inflammationlong acting human GHulcerative colitis

Identifiers

PMID28946616
PMCPMC5666728
OpenAlexW2758046320

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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.