galactosemias/potasyòm

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6 rezilta yo

Abnormalities of retinal metabolism in diabetes or galactosemia: ATPases and glutathione.

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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

Galactosaemia and major burn--a case report.

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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

Abnormalities of retinal metabolism in diabetes or experimental galactosemia. VI. Comparison of retinal and cerebral cortex metabolism, and effects of antioxidant therapy.

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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

The inhibition of sodium, potassium-stimulated ATPase and corneal swelling: the role played by polyols.

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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

Combination of glycemic and oxidative stress in lens: implications in augmentation of cataract formation in diabetes.

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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

Mutation analysis of the GLUT2 gene in three unrelated Egyptian families with Fanconi-Bickel syndrome: revisited gene atlas for renumbering.

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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

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