April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Insulin and Eye Growth: Systemic Effects, Interactions with Glucagon and Effects on Spatial Vision
Author Affiliations & Notes
  • Marita P. Feldkaemper
    University of Tuebingen, Institute for Ophthalmic Research, Tuebingen, Germany
  • Eva Burkhardt
    University of Tuebingen, Institute for Ophthalmic Research, Tuebingen, Germany
  • Frank Schaeffel
    University of Tuebingen, Institute for Ophthalmic Research, Tuebingen, Germany
  • Footnotes
    Commercial Relationships  Marita P. Feldkaemper, None; Eva Burkhardt, None; Frank Schaeffel, None
  • Footnotes
    Support  CIN Pool project 2009-05 and MyEuropia European Union Research Program, MRTN-CT-2006-034021
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 6303. doi:
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      Marita P. Feldkaemper, Eva Burkhardt, Frank Schaeffel; Insulin and Eye Growth: Systemic Effects, Interactions with Glucagon and Effects on Spatial Vision. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6303.

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

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Abstract

Purpose: : Glucagon acts as a stop signal for myopia development in chicks whereas insulin acts in the opposite direction. The growth-stimulating effect of insulin is strongly enhanced if the retinal image is degraded by defocus of either sign. To learn more about the mode of action of insulin, we injected insulin into the peritoneum and combinations of glucagon and insulin into the vitreous. Moreover, effects of insulin on contrast sensitivity were studied in vitro, using the microelectrode array (MEA) to record from mouse ganglion cells.

Methods: : Chicks were treated unilaterally with +7D spectacle lenses and injected with insulin (12 nmol) into the peritoneum (2) Chicks were injected with glucagon (1.75 nmol), insulin (0.06 nmol) or a combination of both. Refraction and axial length were measured after 4 days of treatment. (3) Spikes from the ganglion cells of mouse retinae were recorded in response to changes in contrast (spatial stimuli were checkerboard patterns of 0.07 cyc/deg.) Recordings were done with or without insulin in the superfusate (2.45 ng/ml).

Results: : (1) Intraperitoneal (IP) insulin injections, different from intravitreal injections, did not interfere with positive lens induced hyperopia development. Some control eyes got hyperopic after IP insulin injections and intravitreal glucose levels were significantly higher in those hyperopic control eyes compared to controls that were not influenced by the insulin injections. (2) +7D lens-treated and glucagon injected chicks became hyperopic. Insulin not only prevented the compensation of positive lenses but even induced myopia. Chicks became still myopic when insulin and glucagon were combined, but significantly less than with insulin alone. (3) Taking the number of spikes of selected ganglion cells in a one-second time window after phase-reversal of the checkerboard, divided by the number of spikes in the respective time window before, ganglion cell responses increased with contrast but spike rates were generally lower after insulin application, especially at low contrasts (mean decline 70% ±; 24%). This effect was partially reversible.

Conclusions: : Insulin and glucagon act antagonistically on eye growth, but insulin appears more potent. A striking finding was that glucose levels were higher in the vitreous of those control eyes that had developed spontaneous hyperopia after IP insulin injections. Finally, since insulin reduced contrast sensitivity of ganglion cells, it is possible that it interferes with eye growth by changing spatial processing in the retina.

Keywords: refractive error development • myopia • retina 
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