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Glucose and fat are converted to pyruvate in the body. Pyruvate is then transported into the mitochondria where it's then converted to acetyl-CoA by pyruvate dehydrogenase. This study found that adding DCA (which potently enhances pyruvate dehydrogenase (PDH) by inhibiting PDH kinase) to liver cells with pyruvate significantly enhanced ketone production more so compared to caprylic acid.
"Livers perfused with long-chain fatty acids or the medium-chain fatty acid octanoate showed no evidence of ketogenesis in the 13C spectrum. In contrast, addition of dichloroacetate, a potent inhibitor of pyruvate dehydrogenase kinase, resulted in significant production of both acetoacetate and 3-hydroxybutyrate from the pyruvate precursor."
It significantly enhances acetoacetate production and increased the acetoacetate to beta-hydroxybutyrate ratio, which is a great measure for the NAD:NADH ratio. Meaning, that stimulating PDH can dramatically enhance acetoacetate and NAD as well as BHB, which is an HDAC inhibitor. HDAC inhibitors can further enhance PDH function.
Furthermore, the boost in NAD can increase SIRT3 action, which upregulates PDH even more.
I just found this interesting to share that we can make ketones from glucose and not just fat.
Frontiers | Detecting de novo Hepatic Ketogenesis Using Hyperpolarized [2-13C] Pyruvate
The role of ketones in metabolic health has progressed over the past two decades, moving from what was perceived as a simple byproduct of fatty acid oxidatio...
www.frontiersin.org
It significantly enhances acetoacetate production and increased the acetoacetate to beta-hydroxybutyrate ratio, which is a great measure for the NAD:NADH ratio. Meaning, that stimulating PDH can dramatically enhance acetoacetate and NAD as well as BHB, which is an HDAC inhibitor. HDAC inhibitors can further enhance PDH function.
Furthermore, the boost in NAD can increase SIRT3 action, which upregulates PDH even more.
I just found this interesting to share that we can make ketones from glucose and not just fat.