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Specifically, upon GDH1 deletion, the elevated levels of -ketoglutarate, and not those of NADH, resulted in the observed telomeric silencing defects [40]

We could talk about biological mechanisms all day, but if the compound being studied isn't what it claims to be, the entire conversation is moot

Unpublished report from FDRL, Inc., Waverly, New York, USA

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It essentially tells your cells to burn fat for fuel, not just glucose

Glutamine can serve as a nitrogen donor (- and -nitrogen) or a carbon donor, promoting the biosynthesis of important products such as NAD + [127, 128]