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The investigators reported that oral AOD-9604 administration in rodent models produced measurable increases in fat oxidation and reductions in body fat, and that direct application of the compound to ex vivo human adipose tissue produced concentration-dependent increases in lipolysis [2]

Thus, despite stimulated glycolysis, glucose oxidation is noticeably declined in taurine-deficient hearts, which intensely reduces the contribution of glucose metabolism toward overall adenosine triphosphate (ATP) biosynthesis

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However, mTORC1 activation only promoted metabolic reprogramming of Gclc -deficient FoB but was not sufficient to ensure antibody production, in contrast to B cell cells isolated from tuberous sclerosis complex 1 (TSC1)-deficient mice 102

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