Relevant bibliographies by topics / Fructose, Aldolase B

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Academic literature on the topic 'Fructose, Aldolase B'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Fructose, Aldolase B"

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Cox, Timothy M. "Aldolase B and fructose intolerance." FASEB Journal 8, no. 1 (1994): 62–71. http://dx.doi.org/10.1096/fasebj.8.1.8299892.

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SANTAMARIA, Rita, Gabriella ESPOSITO, Luigi VITAGLIANO, et al. "Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase." Biochemical Journal 350, no. 3 (2000): 823–28. http://dx.doi.org/10.1042/bj3500823.

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We have identified a novel hereditary fructose intolerance mutation in the aldolase B gene (i.e. liver aldolase) that causes an arginine-to-glutamine substitution at residue 303 (Arg303 → Gln). We previously described another mutation (Arg303 → Trp) at the same residue. We have expressed the wild-type protein and the two mutated proteins and characterized their kinetic properties. The catalytic efficiency of protein Gln303 is approx. 1/100 that of the wild-type for substrates fructose 1,6-bisphosphate and fructose 1-phosphate. The Trp303 enzyme has a catalytic efficiency approx. 1/4800 that of
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AGIUS, Loranne. "Substrate modulation of aldolase B binding in hepatocytes." Biochemical Journal 315, no. 2 (1996): 651–58. http://dx.doi.org/10.1042/bj3150651.

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The binding properties of hepatic aldolase (B) were determined in digitonin-permeabilized rat hepatocytes after the cells had been preincubated with either glycolytic or gluconeogenic substrates. In hepatocytes that had been preincubated in medium containing 5 mM glucose as sole carbohydrate substrate, binding of aldolase to the hepatocyte matrix was maximal at low KCl concentrations (20 mM) or bivalent cation concentrations (1 mM Mg2+) and half-maximal dissociation occurred at 50 mM KCl. Preincubation of hepatocytes (for 10–30 min) with glucose or mannose (10–40 mM), fructose, sorbitol, dihyd
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Hopgood, M. F., S. E. Knowles, J. S. Bond, and F. J. Ballard. "Degradation of native and modified forms of fructose-bisphosphate aldolase microinjected into HeLa cells." Biochemical Journal 256, no. 1 (1988): 81–88. http://dx.doi.org/10.1042/bj2560081.

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The uptake and degradation of radiolabelled rabbit muscle fructose-bisphosphate aldolase (EC 4.1.2.13) was studied in HeLa cells microinjected by the erythrocyte ghost fusion system. Labelled aldolase was progressively modified by treatment with GSSG or N-ethylmaleimide (NEM) before microinjection to determine whether these agents, which inactivate and destabilize the enzyme in vitro, affect the half-life of the enzyme in vivo. Increasing exposure of aldolase to GSSG or NEM before microinjection increased the extent of aldolase transfer into the HeLa cells and decreased the proportion of the p
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Droppelmann, Cristian A., Doris E. Sáez, Joel L. Asenjo, et al. "A new level of regulation in gluconeogenesis: metabolic state modulates the intracellular localization of aldolase B and its interaction with liver fructose-1,6-bisphosphatase." Biochemical Journal 472, no. 2 (2015): 225–37. http://dx.doi.org/10.1042/bj20150269.

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We have demonstrated that cellular localization of aldolase B and its interaction with fructose-1,6-bisphosphatase-1 (FBPase-1) is modulated by the metabolic conditions. These results show a new level of regulation for aldolase B and FBPase-1 in a cellular context.
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RELLOS, Peter, Manir ALI, Michel VIDAILHET, Jurgen SYGUSCH, and Timothy M. COX. "Alteration of substrate specificity by a naturally-occurring aldolase B mutation (Ala337→Val) in fructose intolerance." Biochemical Journal 340, no. 1 (1999): 321–27. http://dx.doi.org/10.1042/bj3400321.

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A molecular analysis of human aldolase B genes in two newborn infants and a 4-year-old child with hereditary fructose intolerance, the offspring of a consanguineous union, has identified the novel mutation Ala337 → Val in homozygous form. This mutation was also detected independently in two other affected individuals who were compound heterozygotes for the prevalent aldolase B allele, Ala149 → Pro, indicating that the mutation causes aldolase B deficiency. To test for the effect of the mutation, catalytically active wild-type human aldolase B and the Val337 variant enzyme were expressed in Esc
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Develi-Is, Seval, Gulsev Ozen, Seldag Bekpinar, et al. "Resveratrol improves high-fructose-induced vascular dysfunction in rats." Canadian Journal of Physiology and Pharmacology 92, no. 12 (2014): 1021–27. http://dx.doi.org/10.1139/cjpp-2014-0245.

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High levels of fructose in the diet results in metabolic abnormalities and vascular disorders. In this study, the effect of resveratrol (RES) on vascular relaxation and contraction responses was examined in the aorta of high-fructose (HFr)-fed rats. mRNA expressions of aortic sirtuin 1 (SIRT1), GLUT5, and aldolase B were also investigated. Rats were given fructose (30%) and (or) RES (50 mg·L−1) in their drinking water for 8 weeks. In the HFr-fed rats, plasma levels of arginine and the ratio of arginine:asymmetric dimethylarginine (ADMA) decreased, whereas leptin levels increased. Decreased rel
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Simons, Nynke, François-Guillaume Debray, Nicolaas C. Schaper, et al. "Patients With Aldolase B Deficiency Are Characterized by Increased Intrahepatic Triglyceride Content." Journal of Clinical Endocrinology & Metabolism 104, no. 11 (2019): 5056–64. http://dx.doi.org/10.1210/jc.2018-02795.

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Abstract Context There is an ongoing debate about whether and how fructose is involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). A recent experimental study showed an increased intrahepatic triglyceride (IHTG) content in mice deficient for aldolase B (aldo B−/−), the enzyme that converts fructose-1-phosphate to triose phosphates. Objective To translate these experimental findings to the human situation. Design Case-control study. Setting Outpatient clinic for inborn errors of metabolism. Patients or Other Participants Patients with hereditary fructose intolerance, a rare
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De Souza, M., R. Lindeman, F. Volpato, R. J. Trent, and R. Kamath. "Mutation of aldolase B genes in hereditary fructose intolerance." Lancet 335, no. 8693 (1990): 856. http://dx.doi.org/10.1016/0140-6736(90)90969-c.

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BUONO, Pasqualina, Lisa de CONCILIIS, Paola IZZO, and Francesco SALVATORE. "The transcription of the human fructose-bisphosphate aldolase C gene is activated by nerve-growth-factor-induced B factor in human neuroblastoma cells*." Biochemical Journal 323, no. 1 (1997): 245–50. http://dx.doi.org/10.1042/bj3230245.

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A DNA region located at around -200 bp in the 5´ flanking region (region D) of the human brain-type fructose-bisphosphate aldolase (aldolase C) gene has been analysed. We show by transient transfection assay and electrophoretic-mobility-shift assay (EMSA) that the binding of transcriptional activators to region D is much more efficient (80% versus 30%) in human neuroblastoma cells (SKNBE) than in the non-neuronal cell line A1251, which contains low levels of aldolase C mRNA. The sequence of region D, CAAGGTCA, is very similar to the AAAGGTCA motif present in the mouse steroid 21-hydroxylase ge
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Dissertations / Theses on the topic "Fructose, Aldolase B"

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Langhammer, Marcus. "Molekularbiologischer Nachweis seltener Mutationen im Aldolase B Gen. Ein Beitrag zur Diagnostik der hereditären Fructoseintoleranz." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-77248.

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Mutationen im Gen der Aldolase B auf Chromosom 9 führen zur „hereditären“ Fructoseintoleranz (HFI), die nach einer längeren Fructoseexposition zu schweren Leber- und Nierenschäden bis hin zum völligen Versagen dieser Organe führen kann. Zum Ausschluß bzw. zur Bestätigung einer HFI werden seit ca. 20 Jahren hauptsächlich molekularbiologische Verfahren eingesetzt. Dabei zeigte es sich, dass wenige, regional unterschiedlich häufig vorkommende Mutationen (in Deutschland A149P und A174D) bei dem Großteil der Patienten für diese Erkrankung verantwortlich sind. Viele Laboratorien beschränken sich dah
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Stopa, Jack Davis. "Small molecule stabilization of A149P-aldolase, the most prevalent form of aldolase B associated with hereditary fructose intolerance." Thesis, Boston University, 2012. https://hdl.handle.net/2144/31609.

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Thesis (Ph.D.)--Boston University<br>PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>Hereditary fructose intolerance (HFI) is a disease of carbohydrate metabolism caused by aldolase B deficiency. The most common HFI mutation is an alanine to proline substitution at amino acid position 149 (A
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Oppelt, Sarah Ann. "Characterization of the brain as a site of fructose metabolism and of an aldolase B knockout mouse that mimics human hereditary fructose intolerance." Thesis, 2016. https://hdl.handle.net/2144/17053.

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Excessive fructose consumption in Western diets correlates with increases in obesity, insulin resistance, kidney disease, and non-alcoholic fatty liver disease (NAFLD), collectively part of metabolic syndrome (MBS). Liver and kidneys metabolize 50-70% of ingested fructose, but the fate of remaining fructose remains poorly understood. Moreover, the correlation of fructose ingestion with MBS highlights the need for better understanding of whole-body fructose metabolism, in both health and disease. To that end, valid rodent models for fructose metabolism must reflect the same metabolism in humans
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Books on the topic "Fructose, Aldolase B"

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Lachmann, Robin H., and Timothy M. Cox. Disorders of Fructose Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0003.

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Hereditary fructose intolerance is an autosomal recessive disease which is manifest at weaning but formal diagnosis is often delayed until late childhood or adult life. Fructose, sucrose and sorbitol present in offending foods and drinks induce hypoglycaemia, hypophosphatemia, acidosis, hyperuricemia and hypermagnesemia. If unrecognized, the disease causes failure to thrive, a reno-tubular syndrome with nephrocalcinosis, jaundice, and ultimately liver injury. Parenteral administration of fructose or its congeners can be fatal. Molecular analysis of the aldolase B gene has revolutionized diagno
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Book chapters on the topic "Fructose, Aldolase B"

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Cox, Timothy M. "Inborn errors of fructose metabolism." In Oxford Textbook of Medicine, edited by Timothy M. Cox. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0228.

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Most people in developed countries ingest 50 to 100 g fructose equivalents daily in their diet, arising from fructose itself, sucrose, and sorbitol. After rapid carrier-mediated absorption across the intestinal epithelium, fructose is metabolized (mainly in the liver) by the enzymes ketohexokinase (fructokinase), aldolase B, and triokinase, eventually being converted into glucose or glycogen. Dietary sugars—burgeoning constituents in food and drinks worldwide—have undesirable effects on those with limited capacity to metabolize fructose, including severe illness or death in young patients. ‘Fructose malabsorption’ describes incomplete absorption of fructose that is associated with abdominal symptoms and diarrhoea reminiscent of intestinal disaccharidase deficiency. Symptoms occur after ingestion of fructose- or sorbitol-rich foods and drinks such as apple juice, but as yet a convincing genetic cause for this condition has not been found. Symptoms improve when the offending sugars are avoided. Three inborn errors of fructose metabolism are recognized and these disorders are vivid examples of gene–environment interactions: (1) essential or benign fructosuria due to fructokinase deficiency—a very rare disorder with apparently no ill effects; (2) hereditary fructose intolerance (fructosaemia)—an autosomal recessive disease caused by deficiency of aldolase B; and (3) fructose-1,6-diphosphatase deficiency —a very rare disease of infancy and childhood associated with failure of hepatic gluconeogenesis causing bouts of severe hypoglycaemia, ketosis, and lactic acidosis provoked by infection and starvation.
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Cox, T. M. "Inborn errors of fructose metabolism." In Oxford Textbook of Medicine. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.120302_update_001.

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Most people in developed countries ingest 50 to 150 g fructose equivalents daily in their diet and the use of this sugar in food and drinks is increasing globally. Fructose is absorbed rapidly by a carrier mechanism that facilitates transport across the intestinal epithelium, metabolized (mainly in the liver) by the enzymes ketohexokinase (fructokinase), aldolase B, and triokinase, and eventually converted into glucose or glycogen. Dietary sugar has particular effects on those whose capacity to metabolise fructose is limited. Fructose occurs either as a free monosaccharide, as a component of sucrose, a disaccharide from which it is released by digestion; fructose may also be derived from the metabolism of the sugar alcohol, sorbitol....
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