Disease relevance of GLUD1

• Body weights and efficiency of feed utilization were depressed and the activity of serum SDH and GDH and the concentration of uric acid were significantly increased [1].
• These data suggest 1) that acidosis increases gluconeogenesis from Gln and Ala by accelerating the glutamate deamination process, and 2) that the glutamate originating from glutamine and alanine are segregated in two different pools within the mitochondria with different access to glutamate dehydrogenase activity [2].

High impact information on GLUD1

• Bromofuroate, an inhibitor of glutamate dehydrogenase, blocked oxidation of glutamate and of glutamine whereas aminoxyacetate, a transaminase inhibitor, had little or no effect with either substrate [3].
• The matrix fraction contained over 74% of the glutamine synthetase activity and the major proportion of the matirx marker enzymes, malate dehydrogenase (71%), NADP-dependent isocitrate dehydrogenase (83%), and glutamate dehydrogenase (57%) [3].
• The localization of a glutaminase activity within avian liver mitochondria plus the absence of an active mitochondrial glutamine transaminase is consistent with the differential effects of the transaminase and glutamate dehydrogenase inhibitors [3].
• Mitochondria isolated from these sources also contain nucleoside diphosphate kinase, malate dehydrogenase, and glutamate dehydrogenase or 3-OH-butyrate dehydrogenase [4].
• Nicotinamide adenine dinucleotide phosphate-specific glutamate dehydrogenase of Neurospora [5].

Biological context of GLUD1

• Liver and kidney function tests included serum SDH, GDH, GOT, total protein, potassium and other serum constituents in addition to total tissue lipids and hematology [6].
• We determined the nucleotide sequence of chicken GDH cDNA and showed that the GDH transcript was widely expressed in the chicken organs [7].

Anatomical context of GLUD1

• Addition of insulin to serum-containing medium increased the level of GS and GDH activities in glial cells prepared from 14-15-day-old embryonic mice [8].
• The muscle cells showed strong activity for cholinesterase and glutamate dehydrogenase and low activity for monoaminoxidase [9].
• We also prepared crude GDH from the nuclear and mitochondrial fractions obtained by subcellular fractionation of the chicken liver cells [7].
• The activitiy levels of succinate dehydrogenase, glutamate dehydrogenase and pyruvate dehydrogenase in the fore, mid and hind brain regions of the thiamine deficient chicken, Gallus domesticus were determined [10].
• Distribution of glutamate dehydrogenase and glutamine synthetase activity in the sheep and chicken digestive tract [11].

Associations of GLUD1 with chemical compounds

• Bromofuroate, inhibitor of glutamate dehydrogenase, had little or no effect; and glutamate oxidation was also inhibited by aminooxyacetate, while it was not affected by DON [12].
• The results suggest that measurement of enzyme activities indicative of liver damage in birds, particularly AST, LDH, and GDH, is a valuable tool in the diagnosis of fatty liver-hemorrhagic syndrome in a flock of layers [13].
• Those changes coincided with significant increases in concentrations of plasma total protein and the enzymes aspartate aminotransferase, glutamate dehydrogenase and gamma-glutamyltransferase, and a decrease in creatinine [14].
• The activities of hexokinase, glucokinase, phosphofructokinase, glucose-6-phosphate dehydrogenase, citrate synthase, glycogen synthetase, glutamate dehydrogenase and aspartate transaminase were measured at 4, 8 and 20 weeks of age [15].
• To contribute to our understanding of nitrogen metabolism in the developing chick we have studied in liver, intestine and yolk sac membrane the ontogeny of both aspartate- and alanine transaminases, glutamate dehydrogenase, adenylate deaminase, glutamine synthetase and xanthine dehydrogenase activities [16].

Other interactions of GLUD1

• Optimum assay conditions for measurement of glutamate oxaloacetate transaminase, glutamate dehydrogenase, sorbitol dehydrogenase, and cholinesterase in avian plasma were developed for the study [17].

Analytical, diagnostic and therapeutic context of GLUD1

• We examined the localization of TM and GDH by immunohistochemistry and revealed that they were distributed in the cytoplasm of the adult chicken liver [7].
• Semi-nondenaturing 2D-PAGE revealed that partially purified GDH from the nuclear fraction was associated with TM, but not GDH from the mitochondrial fraction, suggesting preferential binding of TM to GDH [7].

References