[Propionic acidemia and sodium dipropylacetate].
After administering sodium dipropylacetate to normal rats and biotin-deficient rats, we observed a slight hyperglycinemia, significant constant hyperglycinuria, but no accumulation of propionic acid in the blood or significant urinary elimination. Hepatic propionyl-CoA carboxylase activity, in vivo and in vitro, did not change, neither did sodium dipropylacetate inhibit propionyl-CoA carboxylase nor induce propionic acidemia resulting from a deficiency in this enzyme.
D000214:Acyl Coenzyme A; D000818:Animals; D001710:Biotin / Q000172:deficiency*; D001786:Blood Glucose / Q000378:metabolism; D005998:Glycine / Q000097:blood / Q000652:urine; D008025:Ligases / Q000378:metabolism; D008099:Liver / Q000201:enzymology; D008297:Male; D011422:Propionates / Q000378:metabolism*; D051381:Rats; D014635:Valproic Acid / Q000494:pharmacology*
D000214:Acyl Coenzyme A; D001786:Blood Glucose; D011422:Propionates; D014635:Valproic Acid; D001710:Biotin; D008025:Ligases; D005998:Glycine
Acidémie propionique et dipropylacétate de sodium.