Elhassan 2017 J Endocr Soc
Elhassan YS, Philp AA, Lavery GG (2017) Targeting NAD+ in metabolic disease; new insights into an old molecule. J Endocr Soc 1:816β35. |
Β» Open Access
Elhassan YS, Philp AA, Lavery GG (2017) J Endocr Soc
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-ADP 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, non-alcoholic 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 will precis the accumulating evidence for targeting NAD+ metabolism in metabolic disease, map the different NAD+ boosting strategies and discuss 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.
β’ Bioblast editor: Kandolf G β’ O2k-Network Lab: UK Birmingham Lavery GG
Labels: MiParea: Respiration, mt-Medicine