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Peter F. Kador, PhD; Yukio Takahashi, MD, PhD; Milton Wyman, DVM; Frederick Ferris III, MD
Bethesda, Md

Arch Ophthalmol. 1993;111(5):585.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.

—We thank Engerman for reading and responding to our recent publications in the ARCHIVES involving studies conducted in dogs fed galactose long-term and are happy to respond. As a pioneer in using the dog as an animal model for retinal changes associated with diabetes, Engerman has established the validity of both the diabetic and galactose-fed dog as appropriate models of human diabetic retinopathy. Clearly, the major biochemical link between the initial lesions observed in the diabetic dog and the galactose-fed nondiabetic dog is the aldose reductase-catalyzed conversion of excess intracellular glucose or galactose to their respective sugar alcohols. Based on Engerman's initial observations, we initiated a series of long-term studies in dogs.

Our studies were designed to clarify the initiating lesions and progression of diabetic retinopathy through a combination of histologic and clinical techniques. These have documented the progression of retinal lesions from background retinopathy through advanced retinopathy . . . [Full Text PDF of this Article]

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