Retinopathy in galactosemic dogs continues to progress after cessation of galactosemia
R. L. Engerman and T. S. Kern
Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison.
BACKGROUND: Progression of diabetic retinopathy in human subjects and
animal models is difficult to halt promptly by intensified insulin therapy
and strict glycemic control. OBJECTIVE: To learn whether this resistance to
arrest is peculiar to diabetes and insulin therapy or is a characteristic
of hyperglycemia itself, we have determined the effect of intervention on
diabetic-like retinopathy in a non-diabetic animal model, the galactose-fed
dog. METHODS: Dogs were given a 30% galactose diet. At the end of 24
months, the dogs were divided into two groups, one of which continued to
receive the galactose diet, while the second immediately began receiving
the diet minus galactose. All animals were killed after 60 months of study.
RESULTS: Consumption of the galactose-rich diet resulted, as expected, in
galactosemia evident by elevated hemoglobin A1, plasma nonenzymatically
glycated protein, and erythrocyte polyol concentrations, each of which
decreased to normal levels following withdrawal of dietary galactose.
Retinopathy was found to be equivocal at the end of 24 months of the
galactose diet and subsequently progressed significantly despite cessation
of the galactose diet. CONCLUSION: The fact that retinopathy did not halt
promptly at intervention is consistent with previous data from diabetic
dogs and suggests that the vascular lesions may be due to sequelae of
excessive tissue aldohexose that are not promptly corrected by correction
of the aldohexose level.
