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Results for “GALACTOSEMIA”

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At least 1,117 records · Page 62Linked to original sources
PubMed1998

Retinal vessel changes in galactose-fed dogs.

BACKGROUND: Retinal lesions similar to those in human early-stage diabetic retinopathy have been reported to occur in dogs fed galactose for long periods. Investigations of retinal changes, however, have been limited to studies of the intact retinal vasculature isolated by trypsin digestion. OBJECTIVE: To document the onset and progression of retinal lesions in galactose-fed dogs by the common clinical techniques of fundus color photography and fluorescein angiography. METHODS: Fourteen 6-month-old male beagles made aphakic in 1 eye were divided into a control group (4 dogs), receiving a diet containing 30% cellulose, and a galactosemic group (10 dogs), receiving a diet containing 30% galactose. The progression of retinal changes in these dogs was periodically monitored by color fundus photography and fluorescein angiography. RESULTS: Dogs fed a 30% galactose diet for 28 to 41 months were observed by fluorescein angiography and color fundus photography to develop, in order of frequency, microaneurysms, retinal hemorrhages, intraretinal microvascular abnormalities, retinal nonperfused areas, and varicose and serpiginous veins. These findings are similar to the early clinical retinal changes observed in humans with diabetes. CONCLUSION: These results confirm that galactosemic dogs are an appropriate and suitable animal model for investigating human diabetic retinopathy.

Animals↗
PubMed1972

Sugar cataract.

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Cataract↗
PubMed1980

Presenile cataract formation and decreased activity of galactosemic enzymes.

One hundred forty-seven patients, 144 with advanced cataract formation, had determinations of erythrocyte galactokinase and galactose-1-phosphate uridyl transferase performed. Significant reduction (more than 2 SDs) of one of these enzymes was found in 47.4% of patients 50 years old or less with presenile "idiopathic" bilateral cataracts, 7.1% of other patients with cataracts aged 50 years or less, and 3.8% of patients with cataracts aged 51 years or more. The differences between the group with presenile idiopathic cataracts and the other groups were statistically highly significant (P less than .001). Patients with reduced activity of galactokinase or galactose-1-phosphate uridyl transferase (presumed heterozygotes) compose about 1% of the general population, appear to be more susceptible to idiopathic presenile cataract formation, and may be more prone to secondary cataract formation after a variety of lenticular insults. Dietary restriction of milk and milk products may prevent or delay cataract formation in these individuals.

Adult↗
PubMed1996

A mouse model of diabetic retinopathy.

OBJECTIVE: To obtain a model of diabetic retinopathy to which modern methods of genetic engineering may be applied, by determining the response of 2 strains of mice to long-term galactose feeding. METHODS: Both C57BL/6 mice BALB/c mice were fed each of 2 galactose-rich diets (30% and 50% galactose), and trypsin digests of their retinas were compared with those of controls at durations of up to 26 months. RESULTS: The mortality rate in galactose-fed animals was lower in C57BL/6 mice than in BALB/c mice, and both strains tolerated the 30% galactose diet significantly better than the 50% galactose diet. In C57BL/6 mice fed 30% galactose for 21 to 26 months, saccular microaneurysms were observed in the retina, together with significant increases in the thickness of capillary basement membrane and the prevalence of acellular capillaries and pericyte ghosts. The 50% galactose diet caused significantly more acellular capillaries than normal by 15 months, but excessive mortality precluded study at longer durations. The frequency of acellular capillaries also was greater than normal in BALB/c mice fed 30% galactose for 21 months. Retinal polyol levels in galactose-fed mice were found to be lower than those in galactosemic rats. CONCLUSION: The mouse may provide an inexpensive model suitable for in vivo study of the pathogenesis of diabetic retinopathy using molecular biological techniques.

Aneurysm↗