May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Insulin Has Effects on Chick Eyes Opposite to Those of Glucagon
Author Affiliations & Notes
  • X. Zhu
    Dept of Biology, City College of New York, New York, New York
  • D. Chandrasekar
    School of Optometry, UC Berkeley, Berkeley, California
  • J. Wallman
    Dept of Biology, City College of New York, New York, New York
  • Footnotes
    Commercial Relationships X. Zhu, None; D. Chandrasekar, None; J. Wallman, None.
  • Footnotes
    Support NIH Grants EY 02727 and RR 03060
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 5925. doi:
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      X. Zhu, D. Chandrasekar, J. Wallman; Insulin Has Effects on Chick Eyes Opposite to Those of Glucagon. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5925.

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Abstract
 
Purpose:
 

In chicks, glucagon appears to be a retinal signal involved in lens-compensation: (a) Glucagonergic amacrine cells show opposite modulation of ZENK expression in eyes wearing positive and negative lenses; (b) glucagon and its antagonist inhibit compensation for negative and positive lens-wear, respectively. Because insulin and glucagon act in opposite directions both in metabolic pathways and in control of cell proliferation in chick retina (Fischer et al., 2002, 2005), we ask whether insulin and glucagon are antagonists with respect to eye growth and, if so, whether they act in the same pathway.

 
Methods:
 

Experiment A: Week-old chicks, some wearing binocular +10 D lenses, were injected daily with insulin (doses shown below) in one eye and 20 µl of PBS in the fellow eye. Ocular dimensions were measured with ultrasound daily for 3 days, after which the synthesis of scleral glycosaminoglycans (GAGs) was measured. Experiment B: Chicks without lenses were injected once with 0.01 units of insulin plus 20 nmol of glucagon in one eye, and the same amount of either glucagon (n = 7) or insulin (n = 5) in the fellow eye, and measured 1 day later.

 
Results:
 

Experiment A: Insulin caused a 5-fold increase in the rate of ocular elongation, regardless of lens-wear (see table). In eyes wearing positive lenses, it also increased scleral GAG synthesis and decreased choroidal thickness. Experiment B: To test for interactions between glucagon and insulin, we used a glucagon dose that had a minimal effect on ocular elongation over the next day. Glucagon and insulin injected together caused half as much ocular elongation as in insulin alone (change after 1 day: 63 ± 60 µm vs. 112 ± 45 µm).

 
Conclusions:
 

Insulin has effects opposite to those of glucagon: It increases ocular elongtion and, in eyes wearing positive lenses, it decreases choroidal thickness and increases synthesis of scleral GAGs. Glucagon, at a dose that has a little effect when injected alone, strongly inhibits ocular elongation caused by insulin, suggesting that insulin and glucagon might act on the same pathway.Table: Change (over 3 days) in insulin-injected eyes minus change in fellow eyes  

 
Keywords: emmetropization • choroid • myopia 
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