Evidence map›Paper›PMID 20848206›Full record

ArticleDigestive diseases and sciences2011

Riboflavin depletion impairs cell proliferation in adult human duodenum: identification of potential effectors.

Emi Nakano, Sohail Mushtaq, Paul R Heath, Eun-Sook Lee, Jonathan P Bury, Stuart A Riley, Hilary J Powers, Bernard M Corfe

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2011. 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
0.5field-weighted citation impact, top 34% 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, 43 citations in OpenAlex.

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  13. Role of MicroRNA-423-5p in posttranscriptional regulation of the intestinal riboflavin transporter-3.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Article
  14. Structure/functional aspects of the human riboflavin transporter-3 (American journal of physiology. Cell physiology · 2017
    Article
  15. Article
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  17. Riboflavin transport and metabolism in humans.Journal of inherited metabolic disease · 2016
    Review
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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

8 authors at 3 institutions in 2 countries.

Emi NakanoHuman Nutrition Unit; Faculty of Medicine, Dentistry and Health, The University of Sheffield, Beech Hill Road, Sheffield, S10 2RX, UK. e.nakano@sheffield.ac.uk
Sohail Mushtaq
Paul R Heath
Eun-Sook Lee
Jonathan P Bury
Stuart A Riley
Hilary J Powers
Bernard M Corfe
Unité de Nutrition Humaine · FRUniversity of Sheffield · GBNorthern General Hospital · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C518206/1
6 · The paper itself

Abstract

BACKGROUND AND

aimsRiboflavin (vitamin B2) is an essential dietary component with a known function in oxidative metabolism. Our previous data using a rat model of riboflavin deficiency suggested that riboflavin also functions as a luminal signaling molecule regulating crypt development and cell turnover. Riboflavin deficiency is prevalent in both high- and low-income countries across the globe. This study aims to establish whether riboflavin deficiency has consequences for gastrointestinal (GI) morphology in adults and what the effects and effectors of any such alteration may be.

methodsDuodenal biopsies and blood samples were collected from a cross-section of gastroscopy patients. Crypt morphology and cell division were studied by immunohistochemistry, and biochemical riboflavin status was determined. Additionally a cell culture model of riboflavin deficiency was developed and analyzed using a combination of flow cytometry, and microarray and clonogenic assays.

resultDuodenal crypts from subjects in the lowest quartile of riboflavin status were significantly shorter (P=0.023), less cellular (P=0.007), and had fewer cell divisions (P=0.034) than the crypts of subjects in the top quartile of riboflavin status. Following riboflavin depletion of colon cells in culture, cell cycle slowed. Microscopy revealed impaired mitosis and accumulation of aneuploid cells. Alterations in gene expression profiles reflected this alteration, with several mitosis-related genes altered, including AspM, cyclin B1, and Birc5 downregulated and Kif23 upregulated. Riboflavin depletion in vitro caused irreversible loss of proliferative potential of cells.

conclusionsRiboflavin depletion in adult humans impairs proliferation and proliferative potential of intestinal cells, which may have implications for gastrointestinal function.

Indexed as

Cell ProliferationAdultAgedCaco-2 CellsCross-Sectional StudiesCyclin B1Down-RegulationDuodenumFemaleGastroscopyGene Expression ProfilingHumansInhibitor of Apoptosis ProteinsMaleMicrotubule-Associated ProteinsMiddle AgedASPM protein, humanBIRC5 protein, humanCyclin B1Inhibitor of Apoptosis ProteinsKIF23 protein, humanMicrotubule-Associated ProteinsNerve Tissue ProteinsSurvivin

Identifiers

PMID20848206
OpenAlexW2032404064

What OpenQuestion holds

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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.