rickets/carbohydrate

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[Effect of vitamin D3 and carbostimulin on the content of carbohydrate metabolism substrates and the tricarboxylic acid cycle in liver of rats with experimental rachitis].

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The development of experimental rhachitis in rats is accompanied by a decrease in the dihydroxyacetonephosphate, glyceraldehyde-phosphate concentrations and by an increase in pyruvate, lactate, alpha-ketoglutarate, glutamate, oxalacetate and malate in the liver tissue. The feeding of vitamin D3 and

[Research on energy and carbohydrate metabolism in rickets. Experimental work].

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Glucose Galactose Malabsorption complicated with Rickets and Nephrogenic Diabetes Insipidus.

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Congenital Glucose Galactose malabsorption (CGGM) is a rare disorder with limited data from the Arab world. We report the first case of CGGM in Oman.B.S.A two years old female who presented with chronic osmotic diarrhea since birth with hypernatraemic dehydration. B.S was found to have Glucose

Collagen synthesis and carbohydrate metabolism of rachitic bone.

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1. This paper reports studies on the metabolism of bone from normal chicks and from chicks with vitamin D-deficiency rickets. Both in vitro and in vivo there was an increased incorporation of [(14)C]proline into collagen hydroxyproline by rachitic bone. The proportion of the collagen that was

A Fanconi-Bickel syndrome patient with a novel mutation and accompanying situs inversus totalis.

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Taştemel-Öztürk T, Bilginer-Gürbüz B, Tekşam Ö, Sivri S. A Fanconi-Bickel syndrome patient with a novel mutation and accompanying situs inversus totalis. Turk J Pediatr 2017; 59: 693-695. Fanconi-Bickel syndrome is a rare autosomal recessive disorder of carbohydrate metabolism, caused by mutations

Fanconi-Bickel syndrome: GLUT2 mutations associated with a mild phenotype.

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Fanconi-Bickel syndrome (FBS, OMIM #227810), a congenital disorder of carbohydrate metabolism, is caused by mutations in GLUT2 (SLC2A2), the gene encoding the glucose transporter protein-2. The typical clinical picture is characterized by hepatorenal glycogen accumulation resulting in hepato- and

Chapter 29: historical aspects of the major neurological vitamin deficiency disorders: overview and fat-soluble vitamin A.

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The vitamine doctrine: Although diseases resulting from vitamin deficiencies have been known for millennia, such disorders were generally attributed to toxic or infectious causes until the "vitamin doctrine" was developed in the early 20th century. In the late-19th century, a physiologically

Fanconi-Bickel syndrome as an example of marked allelic heterogeneity.

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Renal tubular acidosis (RTA) encompasses many renal tubular disorders characterized by hyperchloremic metabolic acidosis with a normal anion gap. Untreated patients usually complain of growth failure, osteoporosis, rickets, nephrolithiasis and eventually renal insufficiency. Fanconi-Bickel syndrome

Fanconi-Bickel syndrome versus osteogenesis imperfeeta: An Iranian case with a novel mutation in glucose transporter 2 gene, and review of literature.

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Fanconi-Bickel syndrome is an extremely rare hereditary metabolic disease, characterized by hepatomegaly due to glycogen storage, refractory hypophosphatemic rickets, marked growth retardation and proximal renal tubular acidosis. Recurrent bone fractures are one of the hallmark findings. It is a

Genetic testing of two Pakistani patients affected with rare autosomal recessive Fanconi-Bickel syndrome and identification of a novel SLC2A2 splice site variant.

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Fanconi-Bickel syndrome (FBS) is a rare autosomal recessive carbohydrate metabolism disorder caused by mutations in SLC2A2 encoding the glucose transporter 2 (GLUT2) protein. The clinical manifestations include hepatomegaly, conditional hypo/hyperglycemia, rickets, short stature and proximal renal

Totally vegetarian diets and infant nutrition.

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Observations on the deleterious effects of a totally vegetarian diet in infancy are reported and the difficulties encountered in the prevention of nutritional deficiencies in a vegan religious community are discussed. Twenty-five infants of this community who were seen at the hospital showed

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

Fanconi Bickel Syndrome with Hypercalciuria due to GLUT 2 Mutation.

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BACKGROUND Fanconi Bickel Syndrome is a rare, autosomal recessive, disorder of carbohydrate metabolism. Presence of hypercalciuria is rare. UNASSIGNED 4.5-years-old boy presented with growth failure, hepatomegaly, rickets, fasting hypoglycemia with postprandial hyperglycemia, fanconi syndrome and

A secondary respiratory chain defect in a patient with Fanconi-Bickel syndrome.

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A North African boy, the son of consanguineous parents, presented at 8 years of age with hypophosphataemic rickets due to De Toni-Debré-Fanconi syndrome. Hepatomegaly and abnormalities of carbohydrate metabolism were suggestive of Fanconi-Bickel syndrome. This was confirmed by the detection of a

Scientifically-based strategies for nutrition of the high-risk low birth weight infant.

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Technological advances in the intensive care of low birth weight (LBW) infants have resulted in major increases in their survival. New challenges in meeting their nutritional needs have emerged. Very low birth (VLBW) weight infants have very little body fat or glycogen reserves at birth, making them

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