May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Resistance of Retinal Inflammatory Mediators to Arrest After Re-Institution of Good Glycemic Control in Diabetic Rats
Author Affiliations & Notes
  • R. A. Kowluru
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • P.-S. Chan
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • M. Kanwar
    Ophthalmology, Wayne State Univ/Kresge Eye Inst, Detroit, Michigan
  • Footnotes
    Commercial Relationships  R.A. Kowluru, None; P. Chan, None; M. Kanwar, None.
  • Footnotes
    Support  National Institutes of Health, Juvenile Diabetes Research Foundation, Thomas Foundation, Midwest Eye-Banks and Research to Prevent Blindness.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 1351. doi:https://doi.org/
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      R. A. Kowluru, P.-S. Chan, M. Kanwar; Resistance of Retinal Inflammatory Mediators to Arrest After Re-Institution of Good Glycemic Control in Diabetic Rats. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1351. doi: https://doi.org/.

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

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Abstract

Purpose: : Diabetic retinopathy resists arrest after re-establishment of good glycemic control that has followed a profound period of poor glycemic control, suggesting a ‘metabolic memory phenomenon’. The aim of this study is to elucidate the role of inflammation in the resistance of retinopathy to reverse after termination of hyperglycemia in diabetic rats.

Methods: : Streptozotocin-diabetic rats were randomly divided into 2 groups; group 1 rats remained in poor glycemic control (glycated hemoglobin>11%) for 12 months while group 2 rats were in poor glycemic control for 6 months followed by good glycemic control (glycated hemoglobin<7%) for 6 additional months. Twelve months after initiation of the experiment, retina was isolated for assessment of pro-inflammatory mediators.

Results: : Diabetes increased retinal interleukin (IL)-1β by 2-fold, and its receptor (IL-1R1) by 50% compared to the values obtained for normal rat retina. In the same diabetic rats, tumor necrosis factor (TNF)α was increased by about 3-fold and its receptor, TNF receptor I, by 40%. Further, adhesion molecules, intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1, were elevated by over 40% in the retina in diabetes, and vascular endothelial growth factor (VEGF) was increased by 90%. Reinstitution of good glycemic control for six months that had followed six months of poor control failed to reverse the elevations in IL-1β, TNFα and their receptors. Similar to the cytokines, good glycemic control did not benefit increases in adhesion molecules and VEGF levels.

Conclusions: : Re-establishment of good glycemic control after poor glycemic control does not attenuate diabetes-induced increases in pro-inflammatory mediators. The resistance of retinopathy to reverse after cessation of hyperglycemia may be partly attributed to the failure to suppress inflammatory mediators in the retina.

Keywords: diabetic retinopathy • inflammation 
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