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J Endocr Soc. 2017 May 15;1(7):816-835. doi: 10.1210/js.2017-00092. eCollection 2017 Jul 1.

Targeting NAD+ in Metabolic Disease: New Insights Into an Old Molecule.

Author information

1
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham B15 2TT, United Kingdom.
2
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham B15 2TT, United Kingdom.
3
MRC-ARUK Centre for Musculoskeletal Ageing Research, School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom.

Abstract

Nicotinamide adenine dinucleotide (NAD+) is an established cofactor for enzymes serving cellular metabolic reactions. More recent research identified NAD+ as a signaling molecule and substrate for sirtuins and poly-adenosine 5'-diphosphate polymerases; enzymes that regulate protein deacetylation and DNA repair, and translate changes in energy status into metabolic adaptations. Deranged NAD+ homeostasis and concurrent alterations in mitochondrial function are intrinsic in metabolic disorders, such as type 2 diabetes, nonalcoholic fatty liver, and age-related diseases. Contemporary NAD+ precursors show promise as nutraceuticals to restore target tissue NAD+ and have demonstrated the ability to improve mitochondrial function and sirtuin-dependent signaling. This review discusses the accumulating evidence for targeting NAD+ metabolism in metabolic disease, maps the different strategies for NAD+ boosting, and addresses the challenges and open questions in the field. The health potential of targeting NAD+ homeostasis will inform clinical study design to identify nutraceutical approaches for combating metabolic disease and the unwanted effects of aging.

KEYWORDS:

aging; diabetes; mitochondria; nicotinamide mononucleotide; nicotinamide riboside; nonalcoholic fatty liver disease

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