fructose intolerance/carbohydrate

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Elevated carbohydrate-deficient transferrin (CDT) and its normalization on dietary treatment as a useful biochemical test for hereditary fructose intolerance and galactosemia.

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Abnormalities in protein glycosylation are reported in fructosemia (HFI) and galactosemia, although, particularly in HFI, the published data are limited to single cases. The purpose was to investigate the usefulness of the carbohydrate-deficient transferrin (CDT) profile for identification and

Genetic disorder in carbohydrates metabolism: hereditary fructose intolerance associated with celiac disease.

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Celiac disease (CD) has been associated with several genetic and immune disorders, but association between CD and hereditary fructose intolerance (HFI) is extremely rare. HFI is an autosomal recessive disease caused by catalytic deficiency of aldolase B (fructose-1,6-bisphosphate aldolase). We

[STUDY OF CARBOHYDRATE METABOLISM IN THE COURSE OF HEREDITARY FRUCTOSE INTOLERANCE. ATTEMPT AT INTERPRETATION OF HYPOGLYCEMIA].

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Neutrotoxic effects of fructose administration in rat brain: implications for fructosemia.

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Fructose accumulates in tissue and body fluids of patients affected by hereditary fructose intolerance (HFI), a disorder caused by the deficiency of aldolase B. We investigated the effect of acute fructose administration on the biochemical profile and on the activities of the Krebs cycle enzymes in

Integration of PCR-Sequencing Analysis with Multiplex Ligation-Dependent Probe Amplification for Diagnosis of Hereditary Fructose Intolerance.

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Mutations in the ALDOB gene impair the activity of the hepatic aldolase B enzyme, causing hereditary fructose intolerance (HFI), an inherited autosomic recessive disease of carbohydrate metabolism, that can result in hypoglycemia, liver and kidney failure, coma, and death. Noninvasive diagnosis is

Are heterozygous carriers for hereditary fructose intolerance predisposed to metabolic disturbances when exposed to fructose?

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UNASSIGNED High fructose intake causes hepatic insulin resistance and increases postprandial blood glucose, lactate, triglyceride, and uric acid concentrations. Uric acid may contribute to insulin resistance and dyslipidemia in the general population. In patients with hereditary fructose

Congenital hereditary fructose intolerance and pregnancy.

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Congenital hereditary fructose intolerance is associated with the inability to tolerate fructose and carbohydrates, which are converted into fructose. We describe management of a pregnancy complicated by this disease in the mother and its implications for the neonate.

Hereditary fructose intolerance.

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Hereditary fructose intolerance (HFI) is an inborn error of carbohydrate metabolism that is inherited as an autosomal recessive condition. The disease is caused by a catalytic deficiency of aldolase B and is characterized by severe abdominal symptoms and hypoglycaemia which follow the ingestion of

A partially active mutant aldolase B from a patient with hereditary fructose intolerance.

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Hereditary fructose intolerance (HFI) is a potentially fatal autosomal recessive disease of carbohydrate metabolism. HFI patients are deficient in aldolase B, the isozyme expressed in fructose-metabolizing tissues. The eight protein coding exons, including splicing signals, of the aldolase B gene

Allelic heterogeneity in adult hereditary fructose intolerance. Detection of structural mutations in the aldolase B molecule.

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Hereditary fructose intolerance (HFI) is a disorder of visceral carbohydrate metabolism which is transmitted as a recessive character of moderate to high gene prevalence. The condition is caused by enzymic deficiency of aldolase B and is associated with the synthesis of inactive enzyme protein. The

Identification of a splice-site mutation in the aldolase B gene from an individual with hereditary fructose intolerance.

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Hereditary fructose intolerance (HFI) is a potentially fatal autosomal recessive disease of carbohydrate metabolism. HFI patients exhibit a deficiency of fructose 1-phosphate aldolase (aldolase B), the isozyme expressed in tissues that metabolize fructose. The eight protein-coding exons, including

Microflora and chemical composition of dental plaque from subjects with hereditary fructose intolerance.

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We compared the microbiological and chemical composition of dental plaque from subjects with hereditary fructose intolerance who restrict their dietary sugar intake with that of control subjects who do not. The two groups showed no significant differences in chemical composition of plaque: the mean

Abdominal ultrasonography in inheredited diseases of carbohydrate metabolism.

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OBJECTIVE To determine the usefulness of abdominal sonography in inherited diseases of carbohydrate metabolism. METHODS Thirty patients (age range, 4 months to 27 years) with glycogen storage diseases, galactosemia, disorders of fructose metabolism were studied with sonography. Echogenicity of the

Comparative effects of some carbohydrates on serum sugars, triglycerides and digestive hydrolases.

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For 3 weeks, rats were fed diets containing 60 p. 100 carbohydrate in the form of starch (wheat flour), purified sucrose, commercial sugar or a commercial sweetener containing a mixture of glucose and fructose. Glycemia was lower during the day than at night, and it was lowest in the starch-fed

Carbohydrate-deficient glycoprotein syndromes: inborn errors of protein glycosylation.

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The carbohydrate-deficient glycoprotein (CDG) syndromes (CDGS) are a series of autosomal recessive enzyme deficiencies which result in incomplete glycosylation of plasma proteins. CDGS types Ia and Ib have been related to deficiencies of phosphomannomutase and phosphomannose isomerase, respectively,

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