Declining NAD+, metabolic and mitochondrial function are hallmark features of many patho-physiological processes such as aging and type 2 diabetes. Thus, boosting NAD+ availability may have beneficial and therapeutic potential. NAD+ consumption (e.g. SIRTS) requires its re-synthesis through precursor salvage to maintain appropriate levels. Here we further define a skeletal muscle specific pathway to NAD+ and energy metabolism. Through mRNA and protein expression analysis of NAD+ biosynthesis genes we show that skeletal muscle relies on a limited set of salvage enzymes for NAD+ biosynthesis and replenishment. The most highly expressed and skeletal muscle specific of which is nicotinamide riboside kinase 2 (Nmrk2), which salvages the NAD+ precursor molecule nicotinamide riboside (NR) to produce NAD+.

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