Abstract
Compelling evidence from animal studies (Robison et al, 1989, Notvest and Inserra, 1987; McCaleb et al, 1988, Kador et al 1988; c.f. Dvornik, 1987) and recent results from human clinical trials (Sima et al, 1988; Boulton, 1989) have implicated aldose reductase (AR), the first enzyme in the polyol pathway, in the initiation of a number of the long-term complications of diabetes. These complications develop in tissues where glucose uptake is independent of insulin. In these tissues during diabetes-induced hyperglycemia there is an intense flux of glucose through the polyol pathway which initiates a cascade of biochemical alterations that slowly progress to cell dysfunction and structural damage. While the role of AR in the pathogenesis of diabetic complications is well documented, its physiologic role, if any, under normal glycemic conditions is still unknown.
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© 1990 Plenum Press, New York
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Hohman, T.C., Carper, D., Dasgupta, S., Kaneko, M. (1990). Osmotic Stress Induces Aldose Reductase in Glomerular Endothelial Cells. In: Weiner, H., Wermuth, B., Crabb, D.W. (eds) Enzymology and Molecular Biology of Carbonyl Metabolism 3. Advances in Experimental Medicine and Biology, vol 284. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5901-2_17
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DOI: https://doi.org/10.1007/978-1-4684-5901-2_17
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