Evidence map›Paper›PMID 27667774›Full record

ArticleFood & nutrition research2016

Glucosamine exposure reduces proteoglycan synthesis in primary human endothelial cells in vitro.

Trine M Reine, Trond Geir Jenssen, Svein Olav Kolset

Open access · goldAbstract read
In one paragraph

Article in Food & nutrition research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 93% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. The in vitro effects of aflatoxin BVeterinary medicine and science · 2020
    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

3 authors at 2 institutions in 1 country.

Trine M ReineDepartment of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Trond Geir JenssenSection of Nephrology, Department of Transplant Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Svein Olav KolsetDepartment of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGlucosamine (GlcN) supplements are promoted for medical reasons, for example, for patients with arthritis and other joint-related diseases. Oral intake of GlcN is followed by uptake in the intestine, transport in the circulation and thereafter delivery to chondrocytes. Here, it is postulated to have an effect on synthesis and turnover of extracellular matrix constituents expressed by these cells. Following uptake in the intestine, serum levels are transiently increased, and the endothelium is exposed to increased levels of GlcN. We investigated the possible effects of GlcN on synthesis of proteoglycans (PGs), an important matrix component, in primary human endothelial cells.

methodsPrimary human endothelial cells were cultured in vitro in medium with 5 mM glucose and 0-10 mM GlcN. PGs were recovered and analysed by western blotting, or by SDS-PAGE, gel chromatography or ion-exchange chromatography of (35)S-PGs after (35)S-sulphate labelling of the cells.

resultsThe synthesis and secretion of (35)S-PGs from cultured endothelial cells were reduced in a dose- and time-dependent manner after exposure to GlcN. PGs are substituted with sulphated glycosaminoglycan (GAG) chains, vital for PG function. The reduction in (35)S-PGs was not related to an effect on GAG chain length, number or sulphation, but rather to the total expression of PGs.

conclusionExposure of endothelial cells to GlcN leads to a general decrease in (35)S-PG synthesis. These results suggest that exposure to high levels of GlcN can lead to decreased matrix synthesis, contrary to what has been claimed by supporters of such supplements.

Indexed as

arthritisendothelial cellsglucosamineglycosaminoglycanproteoglycan

Identifiers

PMID27667774
PMCPMC5035772
OpenAlexW2522526567

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LicenceCC BY
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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.