Über die Phosphorylierung der Fructose in der Leber

Leuthardt, F.; Testa, Emilio

doi:10.1002/hlca.19500330660

Cited by 41 publications

(8 citation statements)

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“…Liver glucoki-and defatted nase has a high km (12 mM) for glucose, a very high km (>800 powder and I mM) for fructose, and is not inhibited by glucose-6-P (1). Liver were carried also contains a ketohexokinase (ATP:u-fructose 1-phospho-dialyzed (NH transferase, EC 2.7.1.3) which phosphorylates fructose to yield fructose-phos fructose-i-P (2,4,7,10). Ketohexokinase, sometimes referred DEAE-cellul to as "fructokinase," also acts on u-tagatose and, to a lesser with 0.025 extent, on L-sorbose (12 (16).…”

Section: Methodsmentioning

confidence: 99%

Fructokinase (Fraction IV) of Pea Seeds

Turner¹,

Harrison²,

Copeland³

1977

Plant Physiol.

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A frutokinase (EC 2.7.1.4) was obtained from pea (Pisum sadvum L.) seeds. This enzyme, termed frctookinase (fraction IV), was specific for fructose as substrate and had little activity with glucose or mannose. Excess fructose inhbited the enzyme at the optimum pH (8.2) but not at pH 6.6. MgATP was inhibitory at pH 6.6. The apparent MichelisMenten constants at pH 8.2 were 0.057 mM for fructose and 0.10 mM for MgATP. Mg2+ ions were essential for activity; Mn2+ could partally replace Mg2+. Fructokinase (fraction IV) had a requirement for K+ ions which could be substantialy replaced by Rb+ or NH4+ but not by Na+. MATERIALS AND METHODSPea seeds obtained fro Glucose-6-P Phosphorylation of hexoses by ATP is usually the initial genase, P-gli reaction in the metabolism of these sugars. There are two NADH, ATI native isoenzymes of yeast hexokinase (ATP:i-hexose 6-phos-6-P-gluconat4 photransferase, EC 2.7.1.1) and these differ with respect to enolpyruvate glucose phosphorylation rates and regulatory properties (1, 11). galactose, L-S Mammalian hexokinases have been separated into four fractions tose, and D-n three of which are inhibited by glucose-6-P (1, 11). The other cal Co., or B fraction is a glucokinase (ATP:1-glucose 6-phosphotransferase, Preparatioi EC 2.7.1.2) originally found in liver (3,13,20). Liver glucoki-and defatted nase has a high km (12 mM) for glucose, a very high km (>800 powder and I mM) for fructose, and is not inhibited by glucose-6-P (1). Liver were carried also contains a ketohexokinase (ATP:u-fructose 1-phospho-dialyzed (NH transferase, EC 2.7.1.3) which phosphorylates fructose to yield fructose-phos fructose-i-P (2, 4, 7, 10). Ketohexokinase, sometimes referred DEAE-cellul to as "fructokinase," also acts on u-tagatose and, to a lesser with 0.025 extent, on L-sorbose (12).EDTA (buffi Plant hexokinases have been known for a considerable period in buffer A u but less definitive information is available. Saltman (14) ex-kinases were tracted hexokinase from several plant tissues and studied some 400 ml 0.27' properties of a preparation from wheat germ. This enzyme buffer A. Fr preparation phosphorylated glucose, fructose, mannose, and collected. Th glucosamine. Wheat germ hexokinases have been purified and the fraction I some physicochemical characteristics studied (5, 9). The pres-to approxima ence of a fructokinase (ATP:u-fructose 6-phosphotransferase, (PM-10 mem EC 2.7.1.4) in immature pea seeds was the subject of a brief arations of tl report by Medina and Sols (8 (Pisum sativum L. var. Progress No. 9) were m F. Cooper Ltd., Wellington, New Zealand. dehydrogenase, pyruvate kinase, lactate dehydrolucose isomerase, P-mannose isomerase, NADP, P and other nucleotides, glucose-6-P, fructose-6-P, e, 2-P-glycerate, 3-P-glycerate, 2,3-P2-glycerate, P-tris, MES, D-fructose, D-glucose, D-mannose, Dsorbose, 2-deoxy-D-glucose, D-glucosamine, D-taganannoheptulose were obtained from Sigma Chemiloehringer Mannheim GmbH. n of Fructokinase IV. Pea seeds were finely ground with ether (16). Extraction of th...

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Section: Methodsmentioning

confidence: 99%

Fructokinase (Fraction IV) of Pea Seeds

Turner¹,

Harrison²,

Copeland³

1977

Plant Physiol.

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“…Fructose is phosphorylated by ketohexokinase and adenosine triphosphate (ATP) to fructose-iphosphate (5)(6)(7)(8)(9)(10), which is converted to dihydroxyacetone phosphate and D-glyceraldehyde by liver aldolase (11)(12)(13), the enzyme Rutter called "aldolase 1-B" (14). Dihydroxyacetone phosphate may enter the glycolytic pathway.…”

Section: Introductionmentioning

confidence: 99%

Enzymes of fructose metabolism in human liver

Heinz¹,

Lamprecht²,

Kirsch³

1968

J. Clin. Invest.

127

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A B S T R A C T The enzyme activities involved in fructose metabolism were measured in samples of human liver. On the basis of U/g of wet-weight the following results were found: ketohexokinase, glycerol kinase, 0.62. Sorbitol dehydrogenases (25.0 U/g), hexosediphosphatase (4.06 U/g), hexokinase (0.23 U/g), and glucokinase (0.08 U/g) were also measured. Comparing these results with those of the rat liver it becomes clear that the activities of alcohol dehydrogenases (NAD and NADP) in rat liver are higher than those in human liver, and that the values of ketohexokinase, sorbitol dehydrogenases, and hexosediphosphatase in human liver are lower than those values found in rat liver. Human liver contains only traces of glycerate kinase.The rate of fructose uptake from the blood, as described by other investigators, can be based on the activity of ketohexokinase reported in the present paper. In human liver, ketohexokinase is present in a four-fold activity of glucokinase and Requests for reprints should be addressed to Dr.

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“…In normal terms, fructose is phosphorylated by fructokinase to fructose 1-phosphate, which is converted to D-glyceraldehyde by aldolase B (Leuthardt and Testa 1951, Hers and Kusaka 1953, Leuthardt and Wolf 1954, Adelman et al 1967 (Fig. 1).…”

Section: Biochemical Findingsmentioning

confidence: 99%

D-glyceric aciduria

Dimer

Schuck

Streck

et al. 2015

An. Acad. Bras. Ciênc.

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Inherited metabolic diseases are a heterogeneous group of diseases caused by a punctual defect in cell metabolism, resulting in the accumulation of toxic intermediate metabolites or in the lack of important biomolecules for adequate cell functioning. D-glyceric aciduria is an inherited disease caused by a deficiency of glycerate 2-kinase activity, whose pathophysiological mechanisms remain unknown. The main clinical and neurological symptoms seen in affected patients include progressive encephalopathy, hypotonia, psychomotor and mental retardation, microcephaly, seizures, speech delay, metabolic acidosis, and even death. In this review we shall discuss these clinical and biochemical findings, as well as diagnosis and treatment of affected patients in order to raise awareness about this condition.

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Über die Phosphorylierung der Fructose in der Leber

Cited by 41 publications

References 10 publications

Fructokinase (Fraction IV) of Pea Seeds

Fructokinase (Fraction IV) of Pea Seeds

Enzymes of fructose metabolism in human liver

D-glyceric aciduria

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