Cold-induced brown adipose tissue (BAT) activation is considered to improve metabolic health. In murine BAT, cold increases the fundamental molecule for mitochondrial function, nicotinamide adenine dinucleotide (NAD), but limited knowledge of NAD metabolism during cold in human BAT metabolism exists. We show that cold increases the serum metabolites of the NAD salvage pathway (nicotinamide and 1-methylnicotinamide) in humans.
View Article and Find Full Text PDFNAD is a redox-active metabolite, the depletion of which has been proposed to promote aging and degenerative diseases in rodents. However, whether NAD depletion occurs in patients with degenerative disorders and whether NAD repletion improves their symptoms has remained open. Here, we report systemic NAD deficiency in adult-onset mitochondrial myopathy patients.
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