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Aldose Reductase in Diabetic Cataracts

Jin H. Kinoshita, PhD; Peter Kador, PhD; Manuel Catiles, MD
JAMA. 1981;246(3):257-261. doi:10.1001/jama.1981.03320030049032.
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AN ASSOCIATION between cataracts and diabetes in humans has been suspected for about two centuries. This in turn has resulted in considerable laboratory research in the development of animal models in which the eye disease process could be studied in detail. From these studies, it was observed that diabetes produced either by pancreatomy or by chemical destruction of beta cells of the pancreas leads to cataracts in dogs, rats, rabbits, monkeys, and other animals. Moreover, the rapidity of cataract development paralleled the severity of the diabetes.1 Thus, this diabetic complication appears directly related to the glucose level.

The cataractous process, first appearing as vacuoles in the equatorial region, proceeds to opacification of the lens nucleus and finally the entire lens (Fig 1). An understanding of the mechanism involved in the development of diabetic cataracts was greatly accelerated by the fact that the process could be duplicated in rats fed


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