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This result contrasts with some previous studies on DSIPs neuroprotective effects that have reported reduction in infarct size in other models [1]

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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]

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