April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
RPE barrier dsyfunction is an early complication in the diabetic eye
Author Affiliations & Notes
  • Zsolt Ablonczy
    Ophthalmology, Medical University of South Carolina, Charleston, SC
  • Danielle Desjardins
    Ophthalmology, Medical University of South Carolina, Charleston, SC
  • Mohammad Dahrouj
    Ophthalmology, Medical University of South Carolina, Charleston, SC
  • Yueying Liu
    Ophthalmology, Medical University of South Carolina, Charleston, SC
  • Kumar Sambamurti
    Neurosciences, Medical University of South Carolina, Charleston, SC
  • Shahid Husain
    Ophthalmology, Medical University of South Carolina, Charleston, SC
  • Craig E Crosson
    Ophthalmology, Medical University of South Carolina, Charleston, SC
  • Footnotes
    Commercial Relationships Zsolt Ablonczy, None; Danielle Desjardins, None; Mohammad Dahrouj, None; Yueying Liu, None; Kumar Sambamurti, None; Shahid Husain, None; Craig Crosson, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1048. doi:
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      Zsolt Ablonczy, Danielle Desjardins, Mohammad Dahrouj, Yueying Liu, Kumar Sambamurti, Shahid Husain, Craig E Crosson; RPE barrier dsyfunction is an early complication in the diabetic eye. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1048.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract 
 
Purpose
 

Diabetes-associated vision loss is often attributed to edema within the layers of the neurosensory retina. The accumulated fluid is commonly thought to be a consequence of leaking neovasular inner retina vessels. However, one of the key functions of the retinal pigment epithelium (RPE) is to actively remove fluid from the retina to keep it relatively dehydrated. Here we investigated the ability of the RPE to resorb fluid in a diabetic rat model.

 
Methods
 

Diabetes was induced in Brown-Norway rats by means of intraperitoneal injections of streptozotocin (STZ, 65 mg/kg in citrate buffer). Glucose, weight, optical coherence tomographs (OCTs), fluorescence angiography, and electroretinography were performed before STZ treatment and at 1, 4, and 8 weeks post-injection. Glucose readings over 250 mg/dL were considered diabetic. Fluid resorption was monitored following the injection of subretinal saline (1 μL) with the blebs imaged using OCT for 1 hour. For each blebs placed, volume was plotted against time and a linear curve fit determined the rate of fluid resorption.

 
Results
 

In STZ-injected animals, blood glucose reached sable levels of 390±50 mg/dL within 72 hours post injection. Sham injected controls had normal (110±25 mg/dL) blood sugar. ERG c-waves began declining at 1 week post injection and continued to decline until 8 weeks. 4 weeks post STZ treatment, fluid resorption by the RPE was decreased (5.6±1.2 µl/cm2*h) compared to sham injected controls (6.5±1.5 µl/cm2*h) and this reduction in RPE fluid transport was significant (3.0±1.6 µl/cm2*h vs. 8.3±0.7 µl/cm2*h) by 8 weeks. However, retina thickness (by OCT) was not altered and vascular features typical of diabetic retinopathy were not detected at any time points.

 
Conclusions
 

These studies provided evidence that the ability of the RPE to remove fluid from the extracellular environment in the neural retina can decline rapidly following the onset of hyperglycemia before typical vascular changes are observed. This reduced resorption ability is likely to be a key factor in the accumulation of fluid within the layers of the retina. Pharmacological inhibitors of this dramatic early decrease in RPE fluid transport are expected to be beneficial to prevent the development of edematous fluid in the retina.

 
 
The removal of subretinal fluid is impaired in diabetic rats.
 
The removal of subretinal fluid is impaired in diabetic rats.
 
Keywords: 499 diabetic retinopathy • 701 retinal pigment epithelium • 505 edema  
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