June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
High glucose modulates thyroid hormone levels in mouse retinal cells
Author Affiliations & Notes
  • Reena Bapputty
    Pediatric Endocrinology, Case Western Reserve University, Cleveland, Ohio, United States
  • Hima Sapa
    Nephrology and Hypertension, Case Western Reserve University, Cleveland, Ohio, United States
  • Masaru Miyagi
    Pharmacology, Case Western Reserve University, Cleveland, Ohio, United States
  • Rose Anne Gubitosi-Klug
    Pediatric Endocrinology, Case Western Reserve University, Cleveland, Ohio, United States
  • Footnotes
    Commercial Relationships   Reena Bapputty None; Hima Sapa None; Masaru Miyagi None; Rose Gubitosi-Klug None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 3588 – A0043. doi:
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      Reena Bapputty, Hima Sapa, Masaru Miyagi, Rose Anne Gubitosi-Klug; High glucose modulates thyroid hormone levels in mouse retinal cells. Invest. Ophthalmol. Vis. Sci. 2022;63(7):3588 – A0043.

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

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Abstract

Purpose : Prior investigations demonstrated that iodothyronine deiodinase (Dio2) gene expression, the enzyme that converts thyroxine (T4) to triiodothyronine (T3), is decreased in the mouse retina during diabetes. As well, exogenous T3 supplementation of primary mouse retinal endothelial cells (mREC) in culture prevented high-glucose induced cell death. Yet, investigations of Dio2 function in mREC under high glucose conditions and the mechanism underlying thyroid hormone effects on the retinal microvasculature have not been studied.

Methods : T4 and T3 were simultaneously quantified by liquid chromatography-tandem mass spectrometry. mREC were cultured in physiologic (5 mM) or high glucose (30 mM). Cell lysates were analyzed after five days in culture for T4 and T3 concentrations. Endothelial nitric oxide synthase (eNOS) was detected in cell lysates by western blotting.

Results : When mREC were grown in the presence of high glucose, intracellular production of T3 decreased and T4 increased leading to a significantly increased T4/T3 ratio (P=0.007) when compared to cells grown in physiologic glucose. Supplementation of cells with T3, but not T4, increased T3 in mREC (P=0.007), consistent with suppressed Dio2 function under high glucose. Similarly, T3, but not T4, supplementation prevented the high glucose-induced rise in eNOS level (P=0.03).

Conclusions : Our study indicates that high glucose during diabetes may cause decreased intracellular T3 concentrations in retinal cells and that may lead to alterations in vascular tone and function, thereby contributing to the pathogenesis of diabetic retinopathy.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

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