EFFECT OF CARNITINE ON MITOCHONDRIAL OXIDATION OF PALMITOYLCARNITINE
EFFECT OF CARNITINE ON MITOCHONDRIAL OXIDATION OF PALMITOYLCARNITINE
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DOI：
10.1042/bj1880451
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发表时间：
1980-01-01
影响因子：
4.1
通讯作者：
HOPPEL, CL
中科院分区：
文献类型：
--
作者：
BRASS, EP;HOPPEL, CL
The effects of carnitine on the metabolism of palmitoylcarnitine were studied by using isolated rat liver mitochondria. Particular attention was given carnitine acyltransferase-mediated interactions between carnitine and the mitochondrial CoA pool. Carnitine concentrations less than 1.25 mM resulted in increased production of acetylcarnitine during palmitoylcarnitine oxidation. Despite this shunting of C2, units to acetylcarnitine formation, no change was observed in the rate of O2 consumption or major product formation (citrate or acetoacetate). No changes were observed in the mitochondrial content of acetyl-CoA, total acid-soluble CoA or acid-insoluble acyl-CoA. These observations support the concept, based on studies in vivo, that the carnitine/acylcarnitine pool is metabolically sluggish and the acyl-group flux is low as compared with the CoA/acyl-CoA pool. Acid-insoluble acyl-CoA content was decreased and CoA content increased at carnitine concentrations > 1.25 mM. When [14C]carnitine was used in the incubations, it was demonstrated that this resulted from acid-insoluble acylcarnitine formation from intramitochondrial acid-insoluble acyl-CoA mediated by carnitine palmitoyltransferase B. The higher carnitine concentrations resulted in no changes in rates of O2 consumption or major product formation. The above effects of carnitine were observed whether citrate or acetoacetate was the major product of oxidation. An increase in acetyl-CoA concentration was observed at high carnitine concentrations only when acetoacetate was the product. Since the rate of acetoacetate production was not changed, these higher acetyl-CoA concentrations suggest that a new steady state had been established to maintain acetoacetate-production rates. Since there was no change in acetyl-CoA concentration when citrate was the major product, a change in the activity of the pathway utilizing acetyl-CoA for ketone-body synthesis and the potential regulation of this pathway must be considered.
