ArticleJournal of diabetes research2014
Effects of fenofibrate on adiponectin expression in retinas of streptozotocin-induced diabetic rats.
Article in Journal of diabetes research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Anti-inflammatory role of fenofibrate in treating diseases.Biomolecules & biomedicine · 2023Review
- The Relationship Between Retinal and Choroidal Thickness and Adiponectin Concentrations in Patients With Type 2 Diabetes Mellitus.Investigative ophthalmology & visual science · 2023Article
- Protective effect ofInternational journal of ophthalmology · 2021Article
- Target Deconvolution of Fenofibrate in Nonalcoholic Fatty Liver Disease Using Bioinformatics Analysis.BioMed research international · 2021Article
- Light-emitting-diode induced retinal damage and its wavelength dependencyInternational journal of ophthalmology · 2017Article
- Central Macular Thickness in Diabetic Macular Edema.Acta endocrinologica (Bucharest, Romania : 2005)Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adiponectin has been associated with increased risks of microvascular complications in diabetes; however, its role in the development of diabetic retinopathy (DR) is unknown. Fenofibrate is a lipid-lowering agent that has been shown to be capable of preventing DR progression. We investigated the expression of adiponectin and its receptors in DR and evaluated the effects of fenofibrate on their expression. The mRNA and protein levels of adiponectin and its receptors were elevated in retinas of streptozotocin-induced diabetic rats and were suppressed following fenofibrate treatment. Immunofluorescence staining demonstrated that adiponectin and adipoR1 were expressed in cells located within blood vessels, the retinal ganglion, and the inner nuclear layer. AdipoR1 was strongly expressed whereas adipoR2 was only weekly expressed in vascular endothelial cells. The in vitro experiments showed that adiponectin expression was induced by high glucose concentrations in RGC-5 and RAW264.7 cells and was suppressed following fenofibrate treatment. AdipoR1 and adipoR2 levels in RGC-5 cells were elevated in high glucose concentrations and suppressed by fenofibrate. Our results demonstrated that adiponectin may be a proinflammatory mediator in diabetic retinas and fenofibrate appears to modulate the expression of adiponectin and its receptors in diabetic retinas, effectively reducing DR progression.
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