When you oxidize in primarily fats, the master conductor redox modulator, which is the NAD to the NADH ratio, specifically in intra mitochondrial one, drops. That ratio basically turns out to be the primary regulator of whether pyrovide dehydrogenase will accept pyrovate and convert into acetyl-CoA or not. So that's really the gist of the random cycle. When you're providing too much of this one micronodron, about the same thing through glucose, if you're providing a lot of glucose, in theory, you should be able to out-compete the free fatty acids, right? But that all depends on how much glucose can get into

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