Diabetic
cataracts are thought to be caused by
hyperglycemia associated with disturbed
glucose metabolism.
Diabetes mellitus often involves abnormal lipid metabolism in addition to abnormal
glucose metabolism. To date, however, very few studies have counted
hyperlipidemia as a risk factor for diabetic
cataracts. The present study was undertaken to determine whether this actually is a risk factor for diabetic
cataracts and to confirm that the onset of
cataracts associated with
diabetes mellitus can be suppressed by correction of
hyperlipidemia. When rats with
streptozotocin (STZ)-induced
diabetes mellitus were fed an ordinary diet,
cataracts became evident at 9 weeks in 26.7% of animals, and increased to an incidence of 73.3% after 10 weeks of STZ treatment. However, in rats with STZ-induced
diabetes mellitus that were fed a
cholesterol rich diet to induce severe
hyperlipidemia,
cataracts were observed one week earlier, after 8 weeks of treatment, in 36.0% of animals, with an increase to a 52.0% incidence and a 76.0% incidence after 9 and 10 weeks of STZ treatment, respectively.
Hyperlipidemia was therefore associated with an earlier onset and an elevated incidence of diabetic
cataracts. When the
lipoprotein lipase (LPL) activator
NO-1886 was administered to diabetic rats which had developed severe
hyperlipidemia, they showed a decrease in plasma total
cholesterol,
triglyceride and non-
high density lipoprotein (non-
HDL)-cholesterol levels and an increase in
high density lipoprotein (
HDL)-cholesterol level, and the onset of diabetic
cataracts was markedly suppressed. The results of this study suggest that
hyperlipidemia and low
HDL-cholesterol levels may be risk factors for the onset of diabetic
cataracts, and that this onset can be suppressed if measures are taken to alleviate these risk factors. The LPL activator
NO-1886 may be useful in preventing the onset of diabetic
cataracts.