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dihydroxyacetone/hypoxie
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Hypoxia up-regulates triosephosphate isomerase expression via a HIF-dependent pathway.
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The glycolytic enzyme triosephosphate isomerase (TPI) catalyses the reversible conversion of dihydroxyacetone phosphate into glyceraldehyde-3-phosphate. We report here that the expression of TPI at both the mRNA and protein levels is increased by hypoxia in vivo and in vitro. The temporal pattern of
Effects of hypoxia of 10-45 seconds duration on energy metabolism in the cerebral cortex of unanesthetized and anesthetized rats.
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Glycolytic and citric acid cycle intermediates, as well as organic phosphates, were measured in the cerebral cortex of unanesthetized rats following arterial hypoxia (administration of 6-8% O2) of 10 and 20 s duration. There were decreases in glucose-6-phosphate and fructose-6-phosphate, and
Some effects of glucose concentration and anoxia on glycolysis and metabolite concentrations in the perfused liver of fetal guinea pig.
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Effects of glucose concentration and anoxia upon the metabolite concentrations and rates of glycolysis and respiration have been investigated in the perfused liver of the fetal guinea pig. In most cases the metabolite concentrations in the perfused liver were similar to those observed in vivo.
Modulating hypoxia-induced hepatocyte injury by affecting intracellular redox state.
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Hypoxia-induced hepatocyte injury results not only from ATP depletion but also from reductive stress and oxygen activation. Thus the NADH/NAD+ ratio was markedly increased in isolated hepatocytes maintained under 95% N2/5% CO2 in Krebs-Henseleit buffer well before plasma membrane disruption
Mechanism of gluconeogenesis inhibition in rat hepatocytes isolated after in vivo hypoxia.
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Gluconeogenesis was studied in hepatocytes isolated from fasted rats submitted to 24 h of hypoxic exposure (inspired O2 fraction 0.1) or to room air. Hepatocytes from hypoxic rats compared with controls exhibited a lower gluconeogenic rate with lactate (5.1 +/- 0.3 vs. 7.2 +/- 0.3 mumol.min-1.g dry
Hypoxic liver injury and the ameliorating effects of fructose: the "glucose paradox" revisited.
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It has been independently postulated that nutritional status is a modulator of the hepatic injury response to hypoxia and that glucose may be a poor substrate for hepatocellular metabolism. This study provides data linking these two concepts within the framework of metabolic zonation of the liver.
Lacking ketohexokinase-A exacerbates renal injury in streptozotocin-induced diabetic mice.
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OBJECTIVE
Ketohexokinase (KHK), a primary enzyme in fructose metabolism, has two isoforms, namely, KHK-A and KHK-C. Previously, we reported that renal injury was reduced in streptozotocin-induced diabetic mice which lacked both isoforms. Although both isoforms express in kidney, it has not been
Control of glycolysis and gluconeogenesis in rat kidney cortex slices.
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1. Glucose uptake or glucose formation has been studied in kidney cortex slices to investigate metabolic control of phosphofructokinase and fructose-diphosphatase activities. 2. Glucose uptake is increased and glucose formation is decreased by anoxia, cyanide or an uncoupling agent. Under these
The Value of Lactate and Pyruvate Measurements in the Assessment of the Redox State of Free Nicotinamide-Adenine Dinucleotide in the Cytoplasm of Perfused Rat Heart.
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In the isolated rat heart perfused with glucose as substrate, measurements were made of perfusate and tissue lactate and pyruvate concentrations, and of tissue α-glycerophosphate and dihydroxyacetone phosphate concentrations. The conditions studied included increased heart work, anoxia, the addition
Regulation of glycolysis and L-glycerol 3-phosphate concentration in rat epididymal adipose tissue in vitro. Role of phosphofructokinase.
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1. Attempts were made to define the role of phosphofructokinase in glycolytic control and the factors regulating the concentration of l-glycerol 3-phosphate in rat epididymal fat pads incubated in vitro. 2. Glycolysis rates were altered by anoxia or by additions of insulin, adrenaline or both to the
Isolation of a FAD-GPDH gene encoding a mitochondrial FAD-dependent glycerol-3-phosphate dehydrogenase from Dunaliella salina.
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The mitochondrial FAD-dependent glycerol-3-phosphate dehydrogenase (FAD-GPDH), recently reported in plants, has been detailed in yeast and animal systems. It oxidizes glycerol-3-phosphate (G-3-P) to dihydroxyacetone phosphate (DHAP) on the outer surface of mitochondrial inner membrane. A cDNA
Evaluation of redox state of isolated perfused rat lung.
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The metabolic responsiveness of lung tissue to inhibition of oxidative metabolism was determined by measurement of the redox state of the isolated perfused and ventilated rat lung. Changes in redox state were evaluated by fluorescence from the lung surface at wavelengths suitable for reduced
Osborn (J) wave appearance on the electrocardiogram in relation to potassium transfer and myocardial metabolism during hypothermia.
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The genesis of the J wave during hypothermia has been attributed to injury current, delayed ventricular depolarization and early repolarization, tissue anoxia, and acidosis. To our knowledge, no studies have addressed the appearance of the J wave in relation to the myocardial K+ transfer and
Hepatocyte injury resulting from the inhibition of mitochondrial respiration at low oxygen concentrations involves reductive stress and oxygen activation.
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By correlating lactate/pyruvate ratios and ATP levels, cytotoxicity induced by the mitochondrial respiratory inhibitors or hypoxia:reoxygenation injury can be attributed not only to ATP depletion but also to reductive stress and oxygen activation. Thus hypoxia, cyanide or antimycin markedly
Effects on intermediary metabolism in mouse tissues by Ro-03-8799.
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Glucose and lipid metabolism in the brain, liver and in a transplanted tumour were found to be variously altered within 2 to 3 h of administering single doses of the radiosensitizer Ro-03-8799 to normal and tumour-bearing mice. Hepatic lactate and glycerol-3-phosphate (G3P) levels were decreased but
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