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doi: 10.1186/s40164-022-00296-9

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In white adipose tissue of obese, insulin-resistant and aged mammals, NNMT is dramatically upregulated and because it consumes both the universal methyl donor (SAM) and the NAD precursor (nicotinamide), its hyperactivity simultaneously depletes the cellular methylation reserve and the NAD-salvage pool [1,2]

For this assay, OCRs were not normalized to protein content, as equal cell numbers were plated and treatments (DMSO, sorafenib, and FCCP) were added just before the measurements began