Diabetes mellitus (DM) is a major health problem with devastating effects on ocular health in both industrialized and developing countries. The control of
hyperglycemia is critical to minimizing the impact of DM on ocular tissues because inadequate
glycemic control leads to ocular tissue changes that range from a temporary blurring of vision to permanent vision loss. The biochemical mechanisms that promote the development of
diabetic complications have been extensively studied. As a result, a number of prominent biochemical pathways have been identified. Among these, the two-step
sorbitol pathway has been the most extensively investigated; nevertheless, it remains controversial. To date, long-term pharmacological studies in animal models of diabetes have demonstrated that the onset and development of ocular complications that include keratopathy, retinopathy and
cataract can be ameliorated by the control of excess metabolic flux through
aldose reductase (AR). Clinically the alleles of AR have been linked to the rapidity of onset and severity of diabetic ocular complications in diabetic patient populations around the globe. In spite of these promising preclinical and human genetic rationales, several clinical trials of varying durations with structurally diverse
aldose reductase inhibitors (ARIs) have shown limited success or failure in preventing or arresting
diabetic retinopathy. Despite these clinical setbacks, topical ARI Kinostat(®) promises to find a home in clinical veterinary ophthalmology where its anticipated approval by the FDA will present an alternative treatment paradigm to
cataract surgery in diabetic dogs. Here, we critically review the role of AR in
diabetes mellitus-linked ocular disease and highlight the development of Kinostat(®) for
cataract prevention in diabetic dogs. In addition to the veterinary market, we speculate that with further safety and efficacy studies in humans, Kinostat(®) or a closely related product could have a future role in treating diabetic keratopathy.