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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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(136) identified a population of neurons that express TRPM2 within the POA that project to corticotropin-releasing hormone neurons in the paraventricular nucleus of the hypothalamus
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