PURPOSE. Feeding dogs a diet containing 30% galactose induces experimental galactosemia and results in the formation of diabetes-like microvascular lesions of the retina. The appearance and progression of these retinal lesions can be arrested in a dose-dependent manner by treating these dogs with aldose reductase inhibitors from the onset of galactosemia. To determine whether the elimination of galactosemia can also reduce the progression of retinal lesions, the galactose diet was removed from the galactosemic dogs after either the appearance of pericyte ghosts or formation of microaneurysms. METHODS. Ten control dogs were fed a normal diet, and 50 dogs were fed a diet containing 30% galactose. The galactose diet was removed from 15 dogs after 24 months, the time at which pericyte ghosts had previously been observed to develop, and from another 15 dogs after 31 months, when microaneurysms had previously been observed to develop. Eighteen dogs were continued on a galactose diet. Beginning at 24 months, eyes from each group were enucleated at approximately 6-month intervals. Changes in retinal lesions were quantified by computer image analyses. RESULTS. Significant (P < 0.05-0-01) increases in the endothelium-pericyte (E-P) ratio and decreases in pericyte density were observed with increased duration of galactose feeding. Although no reversal of retinal lesions occurred, differences in the progression of retinal lesions between the galactose-fed and galactose-deprived groups became evident after 12 to 24 months. CONCLUSIONS. Discontinuation of galactose in the diet at the initial stages of background retinopathy beneficially delays the progression of retinal lesions.
|Original language||English (US)|
|Number of pages||6|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - 2002|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience