Renal metabolism of glutamine in rats with acute renal failure.
Acute renal failure induced by glycerol results in increased metabolism of glutamine by renal cortical slices of rats 16 and 36 hr after onset, and there is also increased glutamine uptake by the kidney in vivo. Metabolism of glutamine and glutamate to glucose is inhibited. At 8 days after onset of renal failure, metabolism of glutamine returns to normal. Initially, activities of phosphate-dependent glutaminase (PDG) and glutamate dehydrogenase are depressed. The activity of glutaminase returns to normal by 8 days, but glutamate dehydrogenase activity is still inhibited. Increased ammoniagenesis and glutamine uptake are mainly a result of increased entry into the cell since activity of glutaminase is inhibited.
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000378:metabolism*; D000818:Animals; D005969:Glutamate Dehydrogenase / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D005972:Glutaminase / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism*; D005990:Glycerol; D007672:Kidney Cortex / Q000378:metabolism*; D051381:Rats
D005971:Glutamates; D005973:Glutamine; D018698:Glutamic Acid; D005969:Glutamate Dehydrogenase; D005972:Glutaminase; D005990:Glycerol