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Description
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]

Metabolic adaptations in the absence of perilipin: increased beta-oxidation and decreased hepatic glucose production associated with peripheral insulin resistance but normal glucose tolerance in perilipin-null mice

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