6 Výsledek
OBJECTIVE
Experimental galactosemia and diabetes are known to result in diabetic-like retinopathy in animals, but the mechanism by which the retinopathy develops remains unclear. Defects of retinal metabolism that are common to galactosemia and diabetes are closely associated with the development of
The management of burns in an adult patient with galactosaemia is described and the problem of lactose-containing drugs in this condition highlighted. The unique problem of hypokalaemia is discussed. Small amounts of lactose contained in various oral drugs which the patient received over a prolonged
Metabolic abnormalities observed in retina and in cerebral cortex were compared in diabetic rats and experimentally galactosemic rats. Diabetes or experimental galactosemia of 2 months duration significantly increased oxidative stress in retina, as shown by elevation of retinal thiobarbituric acid
BACKGROUND
Sodium, potassium-stimulated adenosine triphosphatase (Na,K-ATPase; E. C. 3.6.1.37) is considered to be the principal corneal enzyme responsible for deturgescence. Some metabolites are known to inhibit Na,K-ATPase, including glucose and galactose. In diabetes, some cells take up high
It is well known that the incidence of cataract is higher in diabetics as compared to non-diabetics. Its rate of maturation is also faster in the diabetics. The precise mechanism of this acceleration is not clearly understood. It is hypothesized that this could be a result of the combination of the
BACKGROUND
Fanconi-Bickel syndrome (FBS) is an autosomal recessive disorder caused by defects in the facilitative glucose transporter 2 (GLUT2 or SLC2A2) gene which codes for the glucose transporter protein 2 expressed in hepatocytes and renal tubular cells causing a defect in carbohydrate