Evidence map›Paper›PMID 31541173›Full record

ArticleScientific reports2019

Globally elevating the AGE clearance receptor, OST48, does not protect against the development of diabetic kidney disease, despite improving insulin secretion.

Aowen Zhuang, Felicia Y T Yap, Domenica McCarthy, Chris Leung, Karly C Sourris, Sally A Penfold, Vicki Thallas-Bonke, Melinda T Coughlan, Benjamin L Schulz, Josephine M Forbes

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

10 authors at 4 institutions in 1 country.

Aowen ZhuangGlycation and Diabetes Complications, Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.ORCID http://orcid.org/0000-0002-7409-6629
Felicia Y T YapBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Domenica McCarthyGlycation and Diabetes Complications, Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.
Chris LeungDepartment of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Australia.
Karly C SourrisBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Sally A PenfoldBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Vicki Thallas-BonkeBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Melinda T CoughlanBaker IDI Heart and Diabetes Institute, Melbourne, Australia.ORCID http://orcid.org/0000-0001-8846-6443
Benjamin L SchulzSchool of Chemistry and Molecular Biosciences, University of Queensland, St Lucia, Australia.
Josephine M ForbesGlycation and Diabetes Complications, Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, Australia. Josephine.Forbes@mater.uq.edu.au.ORCID http://orcid.org/0000-0002-5595-8174
Baker Heart and Diabetes Institute · AUTranslational Research Institute · AUThe University of Melbourne · AUThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation of advanced glycation end products (AGEs) have been implicated in the development and progression of diabetic kidney disease (DKD). There has been interest in investigating the potential of AGE clearance receptors, such as oligosaccharyltransferase-48 kDa subunit (OST48) to prevent the detrimental effects of excess AGE accumulation seen in the diabetic kidney. Here the objective of the study was to increase the expression of OST48 to examine if this slowed the development of DKD by facilitating the clearance of AGEs. Groups of 8-week-old heterozygous knock-in male mice (n = 9-12/group) over-expressing the gene encoding for OST48, dolichyl-diphosphooligosaccharide-protein glycosyltransferase (DDOST+/-) and litter mate controls were randomised to either (i) no diabetes or (ii) diabetes induced via multiple low-dose streptozotocin and followed for 24 weeks. By the study end, global over expression of OST48 increased glomerular OST48. This facilitated greater renal excretion of AGEs but did not affect circulating or renal AGE concentrations. Diabetes resulted in kidney damage including lower glomerular filtration rate, albuminuria, glomerulosclerosis and tubulointerstitial fibrosis. In diabetic mice, tubulointerstitial fibrosis was further exacerbated by global increases in OST48. There was significantly insulin effectiveness, increased acute insulin secretion, fasting insulin concentrations and AUC

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease Models, AnimalGene Knock-In TechniquesGlycation End Products, AdvancedHexosyltransferasesInsulinLiver Function TestsMaleMiceStreptozocinDdost protein, mouseGlycation End Products, AdvancedHexosyltransferasesInsulinStreptozocin

Identifiers

PMID31541173
PMCPMC6754370
OpenAlexW2973297570

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.