Insulin acts as a powerful stimulator of axial myopia in chicks

¹ Institute for Ophthalmic Research, Section of Neurobiology of the Eye, Tuebingen, Germany

^* To whom correspondence should be addressed. E-mail: marita.feldkaemper{at}uni-tuebingen.de.

	Abstract

PURPOSE. In animal models, it has been shown that the retina can use the defocus of the projected image to control emmetropization. Glucagon might be involved in the sign of defocus detection, at least in chickens. Since glucagon and insulin often have opposite effects in metabolic pathways, it was tested whether insulin might stimulate eye growth. METHODS. Chicks were treated with either positive or negative spectacle lenses and intravitreally injected with saline, or different amounts of insulin. Refraction, axial length and corneal curvature were measured. Effects of insulin on vitreal glucose concentration, on retinal ZENK and glucagon mRNA levels, and on the number of ZENK-immunoreactive glucagon amacrine cells were studied. RESULTS. ((1) Insulin injections (0.3 nmol) caused only a small myopic shift in control chicks. (2) When positive lenses were worn, insulin (0.3; 0.03 nmol) not only blocked hyperopia but rather induced high amounts of axial myopia. (3) Insulin also enhanced myopia that was induced by negative lenses. (4) Axial elongation was mostly due to an increase in anterior chamber depth and a thickening of the crystalline lens. (5) Insulin temporarily reduced vitreal glucose levels. (6) Insulin increased retinal ZENK mRNA levels whereas the number of ZENK-immunoreactive glucagon amacrine cells was reduced, a finding that is typically linked to myopia development. CONCLUSIONS. Given that insulin is used in the therapy of human metabolic disorders and proposed as an agent to treat corneal epithelial disease, its powerful myopigenic effect, which is mostly due to its effects on the optics of the anterior segment of the eye, merits further investigation.

Key Words: insulin, myopia, refractive error, emmetropization, retina, chick