May 2008
Volume 49, Issue 13
ARVO Annual Meeting Abstract  |   May 2008
Regulation of Insulin Signaling by Beta-adrenergic Receptors in Rat Muller Cells
Author Affiliations & Notes
  • R. J. Walker
    Ophthalmology, Univ of Tennessee - Memphis, Memphis, Tennessee
  • J. J. Steinle
    Ophthalmology, Univ of Tennessee - Memphis, Memphis, Tennessee
  • Footnotes
    Commercial Relationships  R.J. Walker, None; J.J. Steinle, None.
  • Footnotes
    Support  JDRF 2-2006-114; Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 4918. doi:
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      R. J. Walker, J. J. Steinle; Regulation of Insulin Signaling by Beta-adrenergic Receptors in Rat Muller Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4918. doi:

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

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Purpose: : To determine the role of beta-adrenergic receptors in the regulation of insulin signaling in Muller cells

Methods: : For these experiments, rat Müller cells were cultured in both low (5mM) and high glucose (25mM) DMEM medium and 10% FBS. No insulin was present in the medium, but likely in the FBS. To eliminate any insulin from the FBS, cells were starved in the appropriate glycemic conditions but with no FBS added for 18-24 hours. Western blot analysis was completed to determine the protein expression of various components in the insulin signaling cascade.

Results: : Change in glucose environments (low to high) significantly decreased insulin receptor beta activity in cultured rat Müller cells. Results suggest that total IGF-1 receptor, as well as the phosphorylated receptor, is present in rat Müller cells under both low glucose and high glucose conditions but displayed no significant differences. Cells cultured in high glucose displayed a significant decrease in IRS-1 phosphorylation and a significant decrease in the Akt activity, suggesting the loss of an anti-apoptotic signal.

Conclusions: : These results suggest that a decrease in Akt and IRS-1 could possibly be correlated to the decrease in phosphorylation of the insulin receptor in Muller cells cultured in hyperglycemia. Changes in glucose environments exhibited no effects on the phosphorylation of IGF-1 but indicated presence of IGF-1 receptors in both high and low glucose environments. These results indicate that change in glucose environment reduces insulin signaling in cultured rat Muller cells. Future work will characterize insulin signaling modulated by beta-adrenergic receptors.

Keywords: diabetic retinopathy • Muller cells • second messengers 

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