April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Alterations in the corneal nerve in type 2 diabetes: preventive effects of insulin-like growth factor-1 treatment
Author Affiliations & Notes
  • Hiroki Ueno
    Ophthalmology, St Marianna Univ School of Med, Kawasaki, Japan
  • Takaaki Hattori
    Ophthalmology, Tokyo Medical University, Tokyo, Japan
  • Yuta Kumagai
    Ophthalmology, St Marianna Univ School of Med, Kawasaki, Japan
  • Noboru Suzuki
    Immunology and Medicine, St. Marianna University School of Medicine, Kawasaki, Japan
  • Satoki Ueno
    Ophthalmology, St Marianna Univ School of Med, Kawasaki, Japan
  • Hitoshi Takagi
    Ophthalmology, St Marianna Univ School of Med, Kawasaki, Japan
  • Footnotes
    Commercial Relationships Hiroki Ueno, None; Takaaki Hattori, None; Yuta Kumagai, None; Noboru Suzuki, None; Satoki Ueno, None; Hitoshi Takagi, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 489. doi:https://doi.org/
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Hiroki Ueno, Takaaki Hattori, Yuta Kumagai, Noboru Suzuki, Satoki Ueno, Hitoshi Takagi; Alterations in the corneal nerve in type 2 diabetes: preventive effects of insulin-like growth factor-1 treatment. Invest. Ophthalmol. Vis. Sci. 2014;55(13):489. doi: https://doi.org/.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Diabetic keratopathy (DK) remains difficult to be treated. It can cause corneal persistent epithelial defects, suggesting a role of corneal nerves in maintaining the corneal homeostasis. The purpose of this study is to investigate whether corneal nerve is altered in diabetic mice and examine whether the topical application of recombinant human insulin-like growth factor-I (rhIGF-I) normalized these alterations.

Methods: A group consisting of 12-week-old male mice (C57 BLKS db/db mice) with type 2 diabetes mellitus (DM) and a wild-type group were assessed by beta-III tubulin (neural marker) immunostaining. For rhIGF-1 treatment of the diabetic group, 11-week-old ob/ob mice were administered a retrobulbar injection of 100 μg/kg rhIGF-I twice daily for 7 days. On day 7 of the postexperimental procedure, the corneas from diabetic animals were similarly evaluated. In addition, the subbasal density of the corneal nerves was measured in all groups, including rhIGF-1-treated diabetic mice.

Results: Beta-III tubulin expression detected with immunostaining was decreased in the diabetic corneas. Corneal subbasal plexus of nerve fibers with type II DM were preferentially thinner and had fewer branches compared to the normal mice. Compared with the subbasal nerve density in the normal group (58.29 ± 3.94 mm/mm2), a decrease in the diabetic group (27.01 ± 3.70 mm/mm2; P < 0.00001) was observed, whereas the corneal subbasal nerve density significantly increased in the rhIGF-1-treated diabetic group. (38.06 ± 1.67 mm/mm2; P < 0.01).

Conclusions: Our data suggest that corneal subbasal nerve is altered in db/db mice, and rhIGF-I treatment is capable of protecting against corneal damage in type 2 DM. Direct application of rhIGF-1 may serve as an useful strategy for treating severe type 2 DM.

Keywords: 482 cornea: epithelium • 498 diabetes • 615 neuroprotection  
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×