Abstract
Blinding cataract is a significant effect of canine diabetes with 75% of animals affected two years after diagnosis. Lens opacification occurs primarily through the generation of sorbitol, a sugar alcohol, through the action of aldose reductase (AR). The osmotic effect of sorbitol draws water into the lens, causing opacification. Inhibition of AR should thus prevent the generation of cataracts. A topical AR inhibitor has been shown to have this effect, as has the commercially available neutraceutical OcuGLO, containing the AR inhibitor alpha lipoic acid (ALA) together with other plant-based antioxidants. Here a comparison is made between the number of diabetic dogs developing cataracts when given oral ALA alone and those given a mix containing ascorbic acid and tocopherol. Animals given ALA developed significantly fewer lens opacities than those given conventional antioxidants. Cataracts which formed occurred at a significantly greater duration after the commencement of treatment than those on the antioxidant mix. Although this is a small study conducted over a short period, the significant benefit of ALA in diabetic dogs is a reason to evaluate these effects in larger trials. As AR is involved in diabetic retinopathy and neuropathy, this enzyme inhibitor may be worthy of evaluation in preventing these conditions in human diabetics also.
Highlights
The development of blinding lens opacification is widely recognised as a significant problem in diabetic dogs [1]
When glucose in the lens reaches a concentration where the enzyme hexokinase is saturated, another enzyme, aldose reductase, can convert the glucose into sorbitol which has a higher osmotic potential than does glucose. This osmotic gradient draws water into the lens, resulting in a rapid development of cataracts [4]. This generation of lens opacity is generally considered as a rapid event, developing from a clear lens to a mature cataract in a matter of hours or days, generally occurring bilaterally symmetrically
It may be that this is not necessarily the case since veterinary ophthalmologists see diabetic dogs at the point when they have become blind as the second eye progresses from a non-blinding cataract to a mature cataract
Summary
The development of blinding lens opacification is widely recognised as a significant problem in diabetic dogs [1]. When glucose in the lens reaches a concentration where the enzyme hexokinase is saturated, another enzyme, aldose reductase, can convert the glucose into sorbitol which has a higher osmotic potential than does glucose. This osmotic gradient draws water into the lens, resulting in a rapid development of cataracts [4]. Initial changes in lens opacity prior to the development of a mature cataract may occur in diabetic dogs with equatorial vacuoles and cortical opacities occurring in a substantial number of cases, and not necessarily occurring bilaterally symmetrically. Similar changes are seen in dogs experimentally fed galactose [5] and other
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