IOVS Archives of Disease in Childhood
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1167/iovs.08-1702 on July 3, 2008
 (Investigative Ophthalmology and Visual Science. 2009;50:13-23.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.08-1702
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
iovs.08-1702v1
50/1/13    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feldkaemper, M. P.
Right arrow Articles by Schaeffel, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feldkaemper, M. P.
Right arrow Articles by Schaeffel, F.

Insulin Acts as a Powerful Stimulator of Axial Myopia in Chicks

Marita P. Feldkaemper, Irina Neacsu, and Frank Schaeffel

From the Institute for Ophthalmic Research, Section of Neurobiology of the Eye, Tübingen, Germany.

PURPOSE. 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.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2009 by the Association for Research in Vision and Ophthalmology