galactosemias/albumin

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Galactosylated albumin in galactosemia.

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Functional and structural alterations of the glomerular permeability barrier in experimental galactosemia.

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Experimental galactosemia, induced by feeding rats a galactose enriched diet, reproduces many of the neural and ocular complications of diabetes and induces protein glycation and polyol accumulation. To explore the role of these biochemical abnormalities in the pathogenesis of glomerular injury,

In vitro galactation of human serum albumin: analysis of the protein's galactation sites by mass spectrometry.

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The posttranslational modification of proteins by sugars has been demonstrated in diabetes and classical galactosemia. In diabetes, the glycation process occurs as a result of d-glucose nonenzymatically reacting with proteins such as albumin and hemoglobin, used today as important tools to monitor

Glycation of albumin, not glomerular basement membrane, alters permeability in an in vitro model.

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The effects of glycation of either albumin, a plasma protein, or GBM were examined in an in vitro model of GBM permeability. Albumin was incubated with glucose in vitro, and nonglycated and glycated albumin were separated by affinity chromatography. Rat GBM was glycated either in vivo after the

Ultrastructural localization of blood-retinal barrier breakdown in diabetic and galactosemic rats.

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Breakdown of the blood-retinal barrier (BRB) is an early event in diabetic and galactosemic rats, but the location and nature of the specific defect(s) are controversial. Using an electron microscopic immunocytochemical technique, the retinas of normal, diabetic, and galactosemic rats were

Differential Proteomics of Urinary Exovesicles from Classical Galactosemic Patients Reveals Subclinical Kidney Insufficiency.

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Classical galactosemia is caused by a nearly complete deficiency of galactose-1-phosphate uridyltransferase (GALT; EC 2.7.712), resulting in a severely impaired galactose metabolism with galactose-1-phosphate and galactitol accumulation. Even on a galactose-restricted diet, patients develop serious

Discordant effects of the aldose reductase inhibitor, sorbinil, on vascular structure and function in chronically diabetic and galactosemic rats.

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Effects of sorbinil, an aldose reductase inhibitor, were examined on renal glomerular structure, urinary albumin and IgG excretion, and vascular albumin permeation in eyes and aorta of 8-month diabetic, galactose-fed, and age-matched control rats. Sorbinil was added to the diet of one-half of the

[A difficult and complicated case study: neonatal intrahepatic cholestasis caused by citrin deficiency].

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Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is a kind of inborn errors of metabolism, with the main clinic manifestations of jaundice, hepatomegaly, and abnormal liver function indices. As a mitochondrial solute carrier protein, citrin plays important roles in aerobic

Electron microscopic immunocytochemical evidence for the mechanism of blood-retinal barrier breakdown in galactosemic rats and its association with aldose reductase expression and inhibition.

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Blood-retinal barrier (BRB) breakdown occurs in human diabetic retinopathy and can lead to significant loss of vision. The galactosemic rat serves as a model for human diabetic retinopathy and develops many of the same ocular complications, including BRB failure. Aldose reductase (AR), an enzyme in

Aldose reductase and the development of renal disease in diabetic dogs.

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Effects of 5 years administration of an aldose reductase inhibitor (Sorbinil) on renal structure and albumin excretion were evaluated in diabetic dogs. Glycemia, estimated by frequent measurements of HbA1, glycated plasma proteins and glucosuria, was kept comparable between the placebo- and

Metabolic effects of galactose on human HepG2 hepatoblastoma cells.

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HepG2 cells were used as a model system to study the effects of galactose overload on the liver, a target organ of galactose toxicity in patients suffering from transferase-deficient galactosemia. In the presence of galactose, HepG2 cell growth was slow and the pattern of gene expression remained

Neonatal intrahepatic cholestasis caused by citrin deficiency: clinical and laboratory investigation of 13 subjects in mainland of China.

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BACKGROUND Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is a novel inborn error of metabolism due to dysfunction of citrin protein, and much more information about this new disease is still needed for its clinical management. OBJECTIVE To investigate in detail the clinical

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