Acceleration of development of diabetic cataract by hyperlipidemia and low high-density lipoprotein in rats.
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 abnormal lipid metabolism is a risk factor for diabetic cataracts in rats. Cataracts were caused by streptozotocin (STZ) administration in the ordinary diet or cholesterol rich diet fed rats. When rats with STZ (65 mg/kg)-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 53.3% 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 and low high density lipoprotein (HDL) cholesterol, cataracts were observed one week earlier, after 8 weeks of treatment, in 40.0% of animals, with an increase to a 53.3% incidence and an 86.7% incidence after 9 and 10 weeks of STZ treatment, respectively. Plasma glucose levels did not differ between the groups. These results suggest that hyperlipidemia and low HDL cholesterol are associated with an earlier onset and an elevated incidence of diabetic cataracts. We then investigated the relationship between plasma lipids and cataracts by STZ (45-85 mg/kg) administration. The results showed that the onset of cataracts correlated positively with plasma total cholesterol, triglyceride, non-HDL cholesterol and glucose levels, and negatively with HDL cholesterol levels. 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 diabetic cataracts may be accelerated by hyperlipidemia and low HDL cholesterol in rats.
Tsutsumi
K
K
Nutrition Research Institute, Otsuka Pharmaceutical Factory, Inc., Tokushima, Japan.
Inoue
Y
Y
Yoshida
C
C
D000418:Albumins / Q000378:metabolism; D000818:Animals; D001082:Aqueous Humor / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002386:Cataract / Q000097:blood* / Q000209:etiology / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D008076:Cholesterol, HDL / Q000097:blood*; D003921:Diabetes Mellitus, Experimental / Q000097:blood* / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D004435:Eating; D005947:Glucose / Q000378:metabolism; D006949:Hyperlipidemias / Q000097:blood* / Q000150:complications; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood