Also known as: Nicotinamide adenine dinucleotide
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme present in every living cell. NAD+ biology is heavily researched, but most human studies raise NAD+ with precursors such as NR or NMN; studies of NAD+ itself in humans are small.
NAD+ is a coenzyme for cellular redox reactions and is central to mitochondrial function [1]. Sirtuins, PARPs and CD38 consume NAD+, releasing nicotinamide that is recycled mainly through the NAMPT-driven salvage pathway, estimated to supply about 85% of NAD+ in mammals [2]. How directly supplied NAD+ is handled in the body is still being characterized; researchers have measured its plasma and urine metabolites in a small human pilot [3].
| Study | Model | Reported result | Source |
|---|---|---|---|
| NAD+ metabolome during infusion [3] | Human Adults, open-label pilot; plasma and urine metabolites measured (see publication). | Endpoints: plasma and urine NAD+ and metabolites (nicotinamide, methylnicotinamide, ADPR, NMN). Published. | Peer-reviewed Frontiers in Aging Neuroscience 2019 |
| Chronic NAD in high-fat-fed mice [5] | Mouse High-fat-diet model (12-week high-fat diet), C57BL/6 mice, NAD given in final 4 weeks; hypothalamic cells | Researchers reported body-weight and locomotor-rhythm measurements; abstract gives no effect sizes. | Peer-reviewed Obesity 2018 |
| NAD+ metabolism and mitochondria [1] | Review Review of NAD+ metabolism, mitochondria and recent clinical trials | Summarizes NAD+ decline with age and research on precursor- and drug-based approaches to raise it. | Peer-reviewed npj Metabolic Health and Disease 2025 |
| Targeting NAD homeostasis [2] | Review Review of NAD compartments, measurement and modulation | Covers NAD+-consuming enzymes, NAMPT salvage pathway, and precursor studies in mice and humans. | Peer-reviewed Metabolites 2026 |
Human trials are listed for research context only; outcomes are reported in the linked publications. Animal and lab results do not establish effects in humans.
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