[Metabolites of the propionate pathway as regulators of fatty and dicarboxylic acid oxidation in liver mitochondria].
The functioning of the propionate pathway of oxidation substrate metabolism in the norm and under vitamin B12 deficiency has been studied. This pathway has been shown to play an important role in oxidative processes occurring in normal organisms, for its inhibition in B12-deficient animals is associated with a reduction of respiration as well as with noticeable decreases in palmitoylcarnitine and succinate oxidation rates and oxidation phosphorylation coupling. Succinate, the end product of the propionate pathway, normalizes the respiration and restores the rate of palmitoylcarnitine oxidation in B12-deficient animals, which is suggestive of its crucial role in the propionate pathway. In vivo propionate inhibits, whereas methyl malonate stimulates palmitoylcarnitine respiration, however only in intact animals. In B12-deficient animals the sensitivity to these metabolites is decreased.
N I
NI
Fedotcheva
N N
NN
Gessler
S P
SP
Anikeeva
D A
DA
Ignat'ev
V Ia
VIa
Bykhovskiĭ
M N
MN
Kondrashova
D000818:Animals; D003998:Dicarboxylic Acids / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D011422:Propionates / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D014806:Vitamin B 12 Deficiency / Q000378:metabolism
D003998:Dicarboxylic Acids; D005227:Fatty Acids; D011422:Propionates; C029658:propionic acid
Metabolity propionatnogo puti kak reguliatory okisleniia zhirnykh i dikarbonovykh kislot v mitokhondriiakh pecheni.