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Timothy S. Kern, PhD; Ronald L. Engerman, PhD

Arch Ophthalmol. 1996;114(8):986-990.

Abstract
Objective
To obtain a model of diabetic retinopathy to which modern methods of genetic engineering may be applied, by determining the response of 2 strains of mice to long-term galactose feeding.

Methods
Both C57BL/6 mice and BALB/c mice were fed each of 2 galactose-rich diets (30% and 50% galactose), and trypsin digests of their retinas were compared with those of controls at durations of up to 26 months.

Results
The mortality rate in galactose-fed animals was lower in C57BL/6 mice than in BALB/c mice, and both strains tolerated the 30% galactose diet significantly better than the 50% galactose diet. In C57BL/6 mice fed 30% galactose for 21 to 26 months, saccular microaneurysms were observed in the retina, together with significant increases in the thickness of capillary basement membrane and the prevalence of acellular capillaries and pericyte ghosts. The 50% galactose diet caused significantly more acellular capillaries than normal by 15 months, but excessive mortality precluded study at longer durations. The frequency of acellular capillaries also was greater than normal in BALB/c mice fed 30% galactose for 21 months. Retinal polyol levels in galactose-fed mice were found to be lower than those in galactosemic rats.

Conclusion
The mouse may provide an inexpensive model suitable for in vivo study of the pathogenesis of diabetic retinopathy using molecular biological techniques.

Author Affiliations
From the Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison.

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