Insulin acts as a powerful stimulator of axial myopia in chicks.
OBJECTIVE
In animal models, it has been shown that the retina can use the defocus of the projected image to control emmetropization. Glucagon may be involved in the sign of defocus detection, at least in chickens. Since glucagon and insulin often have opposite effects in metabolic pathways, the effect of insulin on eye growth was investigated.


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
Insulin injections (0.3 nmol) caused only a small myopic shift in control chicks. When positive lenses were worn, insulin injections (0.3; 0.03 nmol) not only blocked hyperopia but rather induced high amounts of axial myopia. Insulin also enhanced myopia that was induced by negative lenses. Axial elongation was mostly due to an increase in anterior chamber depth and a thickening of the crystalline lens. Insulin temporarily reduced vitreal glucose levels. Insulin increased retinal ZENK mRNA levels, whereas the number of ZENK-immunoreactive glucagon amacrine cells was reduced, a finding that is typically linked to the development of myopia.


CONCLUSIONS
Given that insulin is used in therapy for human metabolic disorders and has been proposed to treat corneal epithelial disease, its powerful myopiagenic effect, which is mostly due to its effects on the optics of the anterior segment of the eye, merits further investigation.
Feldkaemper
Marita P
MP
Institute for Ophthalmic Research, Section of Neurobiology of the Eye, Tübingen, Germany. marita.feldkaemper@uni-tuebingen.de
Neacsu
Irina
I
Schaeffel
Frank
F
D000199:Actins / Q000235:genetics; D025042:Amacrine Cells / Q000378:metabolism; D000818:Animals; D002645:Chickens; D003315:Cornea / Q000473:pathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D051766:Early Growth Response Protein 1 / Q000235:genetics / Q000378:metabolism; D005123:Eye / Q000254:growth & development; D019084:Fluorescent Antibody Technique, Indirect; D005934:Glucagon / Q000235:genetics / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006956:Hyperopia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007267:Injections; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D009216:Myopia / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D012029:Refraction, Ocular / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012683:Sensory Deprivation; D014822:Vitreous Body / Q000378:metabolism
D000199:Actins; D051766:Early Growth Response Protein 1; D007004:Hypoglycemic Agents; D007328:Insulin; D012333:RNA, Messenger; D005934:Glucagon; D005947:Glucose