De novo NAD⁺ synthesis enhances mitochondrial function and improves health.

ABSTRACT: Nicotinamide adenine dinucleotide (NAD⁺) is a co-substrate for several enzymes, including the sirtuin family of NAD⁺-dependent protein deacylases. Beneficial effects of increased NAD⁺ levels and sirtuin activation on mitochondrial homeostasis, organismal metabolism and lifespan have been established across species. Here we show that α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD), the enzyme that limits spontaneous cyclization of α-amino-β-carboxymuconate-ε-semialdehyde in the de novo NAD⁺ synthesis pathway, controls cellular NAD⁺ levels via an evolutionarily conserved mechanism in Caenorhabditis elegans and mouse. Genetic and pharmacological inhibition of ACMSD boosts de novo NAD⁺ synthesis and sirtuin 1 acti

SUBMITTER: Katsyuba E 

PROVIDER: S-EPMC6448761 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature