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Diabetic and galactosaemic cataracts.

P F Kador, J H Kinoshita

    Ciba Foundation Symposium
    |January 1, 1984
    PubMed
    Summary

    Diabetic cataracts and galactosaemic cataracts share a common cause: the enzyme aldose reductase converts sugars into sugar alcohols. Inhibiting this enzyme prevents sugar cataract formation in animal models.

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    Area of Science:

    • Ophthalmology
    • Biochemistry
    • Metabolic Disorders

    Background:

    • Diabetes mellitus is linked to a higher incidence of cataracts.
    • Diabetic lenses exhibit metabolic changes, including altered electrolyte, glutathione, nucleotide, and sugar levels.
    • Similar biochemical alterations occur in galactosaemic cataracts, suggesting a shared etiology for sugar cataracts.

    Purpose of the Study:

    • To identify the common biochemical pathway initiating sugar cataracts in diabetes and galactosaemia.
    • To investigate the role of aldose reductase in the pathogenesis of sugar cataracts.

    Main Methods:

    • Biochemical analysis of diabetic and galactosaemic lenses.
    • Enzymatic assays to study aldose reductase activity.
    • In vivo studies in animal models to assess cataract prevention.

    Main Results:

    • The enzyme aldose reductase (EC 1.1.1.21) catalyzes the formation of sugar alcohols (polyols) from glucose or galactose.
    • Elevated intracellular polyol levels induce a hyperosmotic effect, leading to lens fiber swelling, vacuole formation, and opacification.
    • Inhibition of aldose reductase effectively prevented sugar cataract formation in animal models.

    Conclusions:

    • Sugar cataracts in diabetes and galactosaemia share a common biochemical origin driven by aldose reductase activity.
    • The accumulation of sugar alcohols is the critical factor in the development of these cataracts.
    • Targeting aldose reductase presents a potential therapeutic strategy for preventing sugar cataracts.

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