Evidence map›Paper›PMID 28465658›Full record

ArticleMolecular vision2017

Impact of obesity with impaired glucose tolerance on retinal degeneration in a rat model of metabolic syndrome.

Kishore Kumar Godisela, Singareddy Sreenivasa Reddy, Chekkilla Uday Kumar, Natarajan Saravanan, Paduru Yadagiri Reddy, Monica M Jablonski, Radha Ayyagari, Geereddy Bhanuprakash Reddy

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

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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.

Kishore Kumar GodiselaNational Institute of Nutrition, Hyderabad, India.
Singareddy Sreenivasa ReddyNational Institute of Nutrition, Hyderabad, India.
Chekkilla Uday KumarNational Institute of Nutrition, Hyderabad, India.
Natarajan SaravananNational Institute of Nutrition, Hyderabad, India.
Paduru Yadagiri ReddyNational Institute of Nutrition, Hyderabad, India.
Monica M JablonskiUniversity of Tennessee, Memphis, TN.
Radha AyyagariShiley Eye Institute, University of California San Diego, La Jolla, CA.
Geereddy Bhanuprakash ReddyNational Institute of Nutrition, Hyderabad, India.
National Institute of Nutrition · INUniversity of California, San Diego · USUniversity of Tennessee Health Science Center · US

Funding

Vision BiostatisticsP30EY022589 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Radha Ayyagari · 2012 to 2026
$10.3M
Molecular Basis of Hereditary Retinal DegenerationsR01EY021237 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI AYYAGARI, RADHA · 2011 to 2020
$5.6M
Genetic Modulators of GlaucomaR01EY021200 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI JABLONSKI, MONICA M · 2011 to 2022
$3.2M
NEI NIH HHS P30 EY022589NEI NIH HHS R01 EY021200NEI NIH HHS R01 EY021237
6 · The paper itself

Abstract

purposeMetabolic syndrome (MetS) is associated with several degenerative diseases, including retinal degeneration. Previously, we reported on progressive retinal degeneration in a spontaneous obese rat (WNIN/Ob) model. In this study, we investigated the additional effect of impaired glucose tolerance (IGT), an essential component of MetS, on retinal degeneration using the WNIN/GR-Ob rat model.

methodsThe retinal morphology and ultrastructure of WNIN/GR-Ob and age-matched littermate lean rats were studied by microscopy and immunohistochemistry. The retinal transcriptome of WNIN/GR-Ob was compared with the respective lean controls and with the WNIN/Ob model using microarray analysis. Expression of selected retinal marker genes was studied via real-time PCR.

resultsProgressive loss of photoreceptor cells was observed in WNIN/GR-Ob rats with an onset as early as 3 months. Similarly, thinning of the inner nuclear layer was observed from 6 months in these rats. Immunohistochemical analysis showed decreased levels of rhodopsin and postsynaptic density protein-95 (PSD-95) proteins and increased levels of glial fibrillary acidic protein (GFAP), vascular endothelial growth factor (VEGF), and calretinin in WNIN/GR-Ob rats compared with the age-matched lean controls, further supporting cellular stress/damage and retinal degeneration. The retinal transcriptome analysis indicated altered expression profiles in both the WNIN/GR-Ob and WNIN/Ob rat models compared to their respective lean controls; these pathways are associated with activation of pathways like cellular oxidative stress response, inflammation, apoptosis, and phototransduction, although the changes were more prominent in WNIN/GR-Ob than in WNIN/Ob animals.

conclusionsWNIN/GR-Ob rats with added glucose intolerance developed retinal degeneration similar to the parent line WNIN/Ob. The severity of retinal degeneration was greater in WNIN/GR-Ob rats compared to WNIN/Ob, suggesting a possible role for IGT in this model. Hence, the WNIN/GR-Ob model could be a valuable tool for investigating the impact of MetS on retinal degeneration pathology.

Indexed as

Disease Models, AnimalAnimalsCalbindin 2Disks Large Homolog 4 ProteinGlial Fibrillary Acidic ProteinGlucose IntoleranceMaleMetabolic SyndromeObesityPhotoreceptor Cells, VertebrateRatsRats, WistarReal-Time Polymerase Chain ReactionRetinal DegenerationRhodopsinVascular Endothelial Growth Factor ACalb2 protein, ratCalbindin 2Disks Large Homolog 4 ProteinDlg4 protein, ratGfap protein, ratGlial Fibrillary Acidic ProteinRhodopsinVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID28465658
PMCPMC5398884
OpenAlexW2605937125

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.