Science of NAD+
Function of NAD+
NAD+ (Nicotinamide Adenine Dinucleotide) is an essential cofactor for enzymes that control the metabolic activity in your cells. Changes in NAD+ levels lead to changes in the functioning of mitochondria, which are the cell’s energy producing organs. Age associated decreases in NAD+ levels cause diminished mitochondrial energy production, leading to metabolic disorders like type-2 diabetes, and non-alcoholic fatty liver disease. NAD+ is also an essential cofactor for enzymes that control DNA repair (enzymes called PARPs), and cellular metabolism (enzymes call Sirtuins).
Low NAD+ in Disease States
Impaired NAD+ mediated Sirtuin signaling in the cell is implicated in the development of insulin resistance and type-2 diabetes [1-7], as well as non-alcoholic fatty liver disease (NAFLD). NAFLD is the most common liver disease in the Western World, leading to inflammation that can progress to cirrhosis or liver cancer. Zhou et al. [8] showed that liver NAD+ levels decline with aging in humans. Evidence suggests that decreased NAD+ dependent Sirtuin action contributes to the formation of NAFLD [9-13]. Human studies are currently being designed to investigate replenishing liver NAD+ levels, thus activating Sirtuins to reverse metabolic dysfunction at the root of NAFLD.
Role of NAD+ in Aging
As we age, NAD+ levels progressively decrease which contributes to the general decline associated with aging [14-15]. Inflammation and oxidation further reduce levels of NAD+ which, in turn, reduces Sirtuin activity. Together, NAD+ and Sirtuins regulate numerous pathways that control our aging and lifespan[17-19]. Mammals contain seven Sirtuin enzymes (SIRT1–7) that have a wide variety of biological functions including control of cellular metabolism and energy, aging and longevity, cell survival, DNA repair, and stress resistance. Boosting cellular NAD+ levels serves as a powerful means to activate Sirtuins, and as a potential therapy for age-related disorders and the general decline associated with aging.
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References
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