Abstract
SCOT is a vital enzyme for tumors: With reference to Carney Triad Cancers and the ketogenic diet
Highlights
Tumor cells have to synthetize fatty acids and lipid membranes, which automatically turns off the degradation of fatty acid and this source of mitochondrial acetylCoA
The works of Eigenbrodt and his team identified the tumor M2 Pyruvate kinase, its persistent phosphorylation closes the last step of glycolysis [1], and the supply of pyruvate, to pyruvate dehydrogenase, which is itself inhibited by phosphorylation; a bottleneck at the end of glycolysis closes the glycolytic acetylCoA supply to the Krebs cycle
Tumor cells become vitally dependent of ketolysis and of the specific ketolytic enzyme succinyl-CoA: 3-oxoacid-CoA transferase (SCOT) to form acetylCoA in their mitochondria [2]
Summary
Tumor cells have to synthetize fatty acids and lipid membranes, which automatically turns off the degradation of fatty acid and this source of mitochondrial acetylCoA. The only possible way to form acetylCoA in tumor cell mitochondria will come from the ketolysis of ketone bodies produced in the liver by ketogenesis. Tumor cells become vitally dependent of ketolysis and of the specific ketolytic enzyme succinyl-CoA: 3-oxoacid-CoA transferase (SCOT) to form acetylCoA in their mitochondria [2].
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