IOVS Journal of Clinical Microbiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
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
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 Reddy, C.
Right arrow Articles by Ghosh, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reddy, C.
Right arrow Articles by Ghosh, S.

Investigative Ophthalmology & Visual Science, Vol 28, 1492-1496, Copyright © 1987 by Association for Research in Vision and Ophthalmology


ARTICLES AND REPORTS

Pathogenesis of experimental lipid keratopathy: corneal and plasma lipids

C Reddy, EL Stock, AD Mendelsohn, HS Nguyen, SI Roth and S Ghosh

Corneal and plasma lipids were studied in a rabbit model to gain insight into the pathogenesis of secondary lipid keratopathy. Rabbits were divided into four groups in which a high cholesterol diet and corneal suture placement were varied to produce lipid keratopathy. In rabbits with lipid keratopathy, quantitative thin layer chromatography revealed that cholesterol esters comprised most of the deposited lipid, with free cholesterol being deposited as well. The ratio of accumulated cholesterol ester to free cholesterol corresponded closely to the same ratio in hypercholesterolemic plasma total low and very low density lipoprotein (TLDL). Furthermore, gas chromatography showed that the cholesterol ester composition in the corneas with lipid keratopathy resembled that seen in hypercholesterolemic plasma TLDL but was different from the pattern observed in the normal cornea. These studies suggest that the direct source of the deposited cholesterol ester is primarily the plasma TLDL. Since phospholipids and triglycerides did not show a significant increase in the experimental corneas, they are presumably metabolized by the keratocytes after the uptake of TLDL. However, the amount of cholesterol ester carried by the lipoprotein exceeds the capacity of the cell for use and excretion and the lipid accumulates in the cornea.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1987 by the Association for Research in Vision and Ophthalmology