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Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...

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Related Experiment Video

Updated: May 9, 2026

Isolation of Primary Mouse Retinal Pigmented Epithelium Cells
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PPARα deficiency exacerbates retinal pathological changes and dysfunction in high-fat diet mice.

Xue Wang1,2,3, Jing-Jing Ding1,4, Chao-Feng Yu3

  • 1Department of Ophthalmology, the Second Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei 230000, Anhui Province, China.

International Journal of Ophthalmology
|June 19, 2025
PubMed
Summary

A high-fat diet worsens retinal dysfunction and pathology in mice lacking peroxisome proliferator-activated receptor-alpha (PPARα). PPARα deficiency exacerbates lipid abnormalities, inflammation, oxidative stress, and cell death in the retina.

Keywords:
electroretinogramhigh-fat dietperoxisome proliferator-activated receptor-alpharetina

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Area of Science:

  • Ophthalmology
  • Metabolic Research
  • Molecular Biology

Background:

  • High-fat diets (HFD) are linked to various metabolic disorders.
  • Retinal dysfunction and pathological changes can occur due to metabolic disturbances.
  • Peroxisome proliferator-activated receptor-alpha (PPARα) plays a role in lipid metabolism.

Purpose of the Study:

  • To investigate the impact of HFD on retinal pathology and function.
  • To determine the role of PPARα in HFD-induced retinal changes using PPARα knockout mice.

Main Methods:

  • Mice (C57BL/6J and PPARα knockout) were fed HFD or standard diet for four months.
  • Retinal triglycerides, malondialdehyde (MDA), and protein/mRNA expression were analyzed.
  • Retinal function was assessed using electroretinography.

Main Results:

  • HFD increased retinal fatty acid oxidation, triglyceride accumulation, and weight.
  • PPARα deficiency exacerbated HFD-induced lipid abnormalities, inflammation (NF-κB pathway), and oxidative stress.
  • HFD-induced retinal ganglion cell (RGC) apoptosis and retinal dysfunction (reduced wave amplitudes) were worsened by PPARα knockout.

Conclusions:

  • PPARα knockout intensifies lipid metabolic abnormalities in the retina under HFD conditions.
  • The absence of PPARα amplifies inflammatory responses, oxidative stress, and apoptosis in HFD-fed mouse retinas.
  • PPARα deficiency significantly contributes to HFD-induced retinal dysfunction.