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The oxidative stress in mitochondria could be counteracted by IDH1-driven reductive carboxylation in the cytosol, followed by the transfer of citrate into the mitochondria, which was to be oxidized by IDH2 to generate NADPH [104]
Together, the stack addresses both energy expenditure (AMPK) and fat accumulation (NNMT inhibition), creating synergistic metabolic effects that neither compound produces alone
However, cell-damage could be induced by abundant production of free radicals that in turn can trigger malfunctions such as cancer or neurodegeneration
In many cases, this protection is incomplete or missing, which greatly increases the risk of damage
Treating diabetes and obesity to improve health outcomes for Americans has become a priority for this administration
